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1.
Pregnancy Hypertens ; 36: 101113, 2024 Jun.
Article in English | MEDLINE | ID: mdl-38490151

ABSTRACT

OBJECTIVE: To compare rates of pregnancy induced hypertensive disorders during the period of the COVID-19 pandemic to prior, baseline years. METHODS: We conducted a retrospective study of 17,742 patients on rates for pregnancy induced hypertensive disorders delivering at 2 local hospitals before (Cohort 1; January 2018 to December 2019; n = 8245) and after (Cohort 2; February 2020 to February 2022; n = 9497) the onset of the COVID-19 pandemic. The primary outcomes were rates of gestational hypertension, pre-eclampsia, and chronic hypertension in patients.Wecompared by year (2018-2022), by patient COVID infection status, and by racial demographics. RESULTS: During the pandemic (Cohort 2), there were lower rates of chronic hypertension (7.4 % vs 6.5 %, p =.02), higher rates of gestational hypertension (26.3 % vs 27.8 %, p =.03), and higher rates of preeclampsia (11.3 % vs 13.1 %, p <.001) compared to years prior to the pandemic (Cohort 1). When evaluating by year, rates of chronic hypertension did not statistically change while rates for preeclampsia increased in the first year of the pandemic and remained high, and rates for gestational hypertension did not increase until the second year of the pandemic. When evaluating by COVID infection status, rates for gestational hypertension were significantly higher for individuals with a positive COVID infection status (COVID negative = 27.4 % vs. COVID positive = 32.8 %; p <.004). Rates of preeclampsia did not differ according to COVID infection status (p = 0.15). CONCLUSION: In this study, rates of pregnancy induced hypertensive disorders increased during the COVID pandemic regardless of COVID infection status.


Subject(s)
COVID-19 , Hypertension, Pregnancy-Induced , Humans , Pregnancy , Female , COVID-19/epidemiology , Hypertension, Pregnancy-Induced/epidemiology , Hypertension, Pregnancy-Induced/ethnology , Adult , Retrospective Studies , SARS-CoV-2 , Pre-Eclampsia/epidemiology , Pre-Eclampsia/ethnology , United States/epidemiology
2.
Cureus ; 13(8): e17500, 2021 Aug.
Article in English | MEDLINE | ID: mdl-34603879

ABSTRACT

Cesarean scar pregnancy (CSP) is a very serious complication of a prior cesarean delivery. The major risks associated with CSP are uncontrolled hemorrhage and uterine rupture, potentially leading to future infertility. Management of CSP remains a major obstetric challenge without a well-defined therapeutic procedure. Dilation & curettage is a commonly used procedure for the treatment of CSP. However, it can be ineffective and often leads to definite infertility. Therefore, we present a case of the successful use of an alternative procedure, Myosure® hysteroscopy, in the treatment of CSP. We herein report the case of a 32-year-old G5P3013 woman who presented with vaginal bleeding and past history of three cesarean sections. She was found to have a CSP with fetal pole and cardiac activity at 6 weeks 2 days. The patient was initially treated with a systemic methotrexate injection, but there was persistence of cardiac activity. A second course of methotrexate was administered into the gestational sac, which systemically led to successful fetal cardiac arrest and downtrend of beta-human chorionic gonadotropin (HCG) level. A dilation & curettage procedure was not successful in removing products of conception. A Myosure hysteroscopy procedure, however, was successful in removing products of conception. The patient was discharged after a negative ultrasound and beta-HCG level. In our review of the literature, we found that there is no general consensus on the management of cesarean scar ectopic pregnancies. To date, there is no literature cited about the use of Myosure for cesarean scar ectopic pregnancies. However, our case suggests that Myosure can be effective for CSP and this warrants a larger-scale controlled study to better evaluate this as a treatment for this condition.

3.
Perm J ; 24: 1-4, 2020 09.
Article in English | MEDLINE | ID: mdl-33482941

ABSTRACT

Women physicians have a long history of advocacy, dating to the 19th century women's suffrage movement. As history recounts the work of the suffragists, many women physicians bear mention. Some were leaders on the national scene, and others led suffrage efforts in their own state. In this article, we provide a snapshot of 7 prominent suffragists who were also physicians: Mary Edwards Walker, Mary Putnam Jacobi, Esther Pohl Lovejoy, Marie Equi, Mattie E. Coleman, Cora Smith Eaton, and Caroline E. Spencer. In sharing their stories, we hope to better understand some of the challenges and struggles of the suffrage movement and how their advocacy paved the way not only for women's voting rights but also the role of women physicians as advocates for change.


Subject(s)
Physicians, Women , Women , Female , History, 20th Century , Humans , Politics , Women's Rights
4.
Invest Ophthalmol Vis Sci ; 57(13): 5338-5347, 2016 Oct 01.
Article in English | MEDLINE | ID: mdl-27727398

ABSTRACT

PURPOSE: To investigate the role of RNA 3'-terminal phosphate cyclase (Rtca) in Toll-like receptor 3 (TLR3)-mediated loss of retinal ganglion cells (RGCs) and their axons. METHODS: Polyinosinic-polycytidylic acid (Poly[I:C]) or PBS was injected into the vitreous humor of C57BL/6J and Tlr3 knockout mice. C57BL/6J mouse eyes were treated with Rtca silencing RNA or control RNA, with or without PBS or Poly(I:C). At 24, 48, and 72 hours after treatments, RGC loss was determined with the brain-specific homeobox/POU domain protein 3a antibody, and axonal loss was assessed by using the neuronal class III beta-tubulin (Tuj1) antibody. Axonal loss in the optic nerves was determined by anterograde-labeling of Cholera Toxin B. Western blot assays were performed to determine TLR3, Rtca, c-jun N-terminal kinase 3 (JNK3), and phospho-JNK3 (pJNK3) levels, and immunohistochemistry assays were performed to determine the cells that synthesize Rtca. RESULTS: Poly(I:C) significantly up-regulated the protein levels of TLR3, Rtca, JNK3, and pJNK3 in the retina. Rtca levels were increased in RGCs, and an increase in Rtca levels promoted significant loss of RGCs and their axons. In Tlr3 knockout mouse retinas, Poly(I:C) failed to elevate Rtca, JNK3, and pJNK3 protein levels and did not promote significant axonal loss. Also, Rtca silencing RNA down-regulated Rtca, JNK3, and pJNK3 in C57BL/6J mouse retinas, and down-regulation of Rtca attenuated Poly(I:C)-mediated loss of RGCs and their axons. CONCLUSIONS: The results presented in this study show that the activation of TLR3 promotes the loss of RGCs and their axons by elevating Rtca levels in the retina. Also, the results presented in this study show that Rtca regulates JNK3 expression in the retina.


Subject(s)
Down-Regulation , Ligases/genetics , Optic Nerve/metabolism , RNA/genetics , Retinal Degeneration/genetics , Retinal Ganglion Cells/pathology , Toll-Like Receptor 3/genetics , Animals , Axons/metabolism , Axons/pathology , Blotting, Western , Disease Models, Animal , Immunohistochemistry , Ligases/metabolism , Mice , Mice, Inbred C57BL , Mice, Knockout , Optic Nerve/diagnostic imaging , Retinal Degeneration/metabolism , Retinal Degeneration/pathology , Retinal Ganglion Cells/metabolism , Toll-Like Receptor 3/biosynthesis
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