Facultad de Enfermería y Fisioterapia Salus Infirmorum

Endometriosis / (Record no. 15055)

MARC details
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003 - CONTROL NUMBER IDENTIFIER
control field OSt
005 - DATE AND TIME OF LATEST TRANSACTION
control field 20230504113148.0
006 - FIXED-LENGTH DATA ELEMENTS--ADDITIONAL MATERIAL CHARACTERISTICS
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007 - PHYSICAL DESCRIPTION FIXED FIELD--GENERAL INFORMATION
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fixed length control field 171219t2019 sp ||||| |||| 00| 0 spa |
022 ## - INTERNATIONAL STANDARD SERIAL NUMBER
International Standard Serial Number 0163-769X
040 ## - CATALOGING SOURCE
Transcribing agency Salus Infirmorum
245 00 - TITLE STATEMENT
Title Endometriosis /
Statement of responsibility, etc. Serdar E. Bulun, Bahar D. Yilmaz, Christia Sison, Kaoru Miyazaki, Lia Bernardi, Shimeng Liu, Amanda Kohlmeier, Ping Yin, Magdy Milad, and JianJun Wei
500 ## - GENERAL NOTE
General note Este artículo se encuentra disponible en su edición impresa.
504 ## - BIBLIOGRAPHY, ETC. NOTE
Bibliography, etc. note Bibliografía: p.1074-1079
520 8# - SUMMARY, ETC.
Summary, etc. Pelvic endometriosis is a complex syndrome characterized by an estrogen-dependent chronic inflammatory process that affects primarily pelvic tissues, including the ovaries. It is caused when shed endometrial tissue travels retrograde into the lower abdominal cavity. Endometriosis is the most common cause of chronic pelvic pain in women and is associated with infertility. The underlying pathologic mechanisms in the intracavitary endometrium and extrauterine endometriotic tissue involve defectively programmed endometrial mesenchymal progenitor/stem cells. Although endometriotic stromal cells, which compose the bulk of endometriotic lesions, do not carry somatic mutations, they demonstrate specific epigenetic abnormalities that alter expression of key transcription factors. For example, GATA-binding factor-6 overexpression transforms an endometrial stromal cell to an endometriotic<br/>phenotype, and steroidogenic factor-1 overexpression causes excessive production of estrogen, which drives inflammation via pathologically high levels of estrogen receptor-b. Progesterone receptor deficiency causes progesterone resistance. Populations of endometrial and endometriotic epithelial cells also harbor multiple cancer driver mutations, such as KRAS, which may be associated with the establishment of pelvic endometriosis or ovarian cancer. It is not known how interactions between epigenomically defective stromal cells and the mutated genes in epithelial cells contribute to the pathogenesis of endometriosis. Endometriosis-associated pelvic pain is managed by suppression of ovulatory menses and estrogen production, cyclooxygenase inhibitors, and surgical removal of pelvic lesions, and in vitro fertilization is frequently used to overcome infertility. Although novel targeted treatments are becoming available, as endometriosis pathophysiology is better understood, preventive approaches such as long-term ovulation suppression may play a critical role in the future.
773 ## - HOST ITEM ENTRY
Related parts -- 2019 v. 40, n 4, p.1048-1079
Title Endocrine Reviews
942 ## - ADDED ENTRY ELEMENTS (KOHA)
Source of classification or shelving scheme Universal Decimal Classification
Koha item type Artículo de revista
Holdings
Withdrawn status Lost status Source of classification or shelving scheme Damaged status Not for loan Collection code Home library Current library Date acquired Total Checkouts Full call number Barcode Date last seen Price effective from Koha item type
    Universal Decimal Classification     Non-fiction Revistas y artículos Revistas y artículos 03/05/2023   PP 6031 03/05/2023 03/05/2023 Artículo de revista

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