The PALM-COEIN classification for causes of abnormal uterine bleeding (AUB) was proposed by the International Federation of Gynecology and Obstetrics (FIGO) in 2011, which has been gradually applied in the diagnosis of AUB in the past 2 years in China. However, there are no reports yet on the causes of chronic AUB among Chinese women with this new classification system.The purpose of this study was to describe the prevalence of the causes of chronic AUB among Chinese women of reproductive age using the PALM-COIEN classification system.This is a cross-sectional study. Beijing Shijitan Hospital, Capital Medical University.A total of 1053 women aged 15 to 55 years with chronic AUB were evaluated between November 2016 and May 2017.Prevalence of the causes of chronic AUB using the PALM-COEIN classification. AUB-O was the most frequent finding in women with chronic AUB, accounting for 608 (57.7%) cases. AUB-P was found in 171 (16.2%) women, AUB-L in 130 (12%) women, AUB-A in 52 (4.94%) women, AUB-E in 28 (2%) women, AUB-I in 23 (2%) women, AUB-M in 20 (1.9%) women, AUB-C in 10 (1%) women, and AUB-N in 10 (0.9%) women.Ovulatory dysfunction (AUB-O) is the most common cause of AUB among the nonstructural causes. Endometrial polyps (AUB-P) are the most common among the structural causes, followed by uterine fibroids (AUB-L) and uterine adenomyosis (AUB-A).
BackgroundIntrauterine adhesion (IUA) is characterized by progressive intrauterine fibrosis as a consequence of trauma to the basal layer of the endometrium. In an attempt to relieve IUA, many approaches have been applied in the clinic but show limited effects. In this study, we investigated the effect of autologous oral mucosal epithelial cells (OMECs) seeded on decellularized and lyophilized amniotic membrane (DL-AM) on preventing the development of IUA in a rat model.MethodsIUA model was established by surgical scraping of the endometrium in the left uteri (the right uteri were kept as control) of SD rats. Wounds were randomly treated as unrepaired (IUA group), repaired with DL-AM alone (DL-AM group), and DL-AM seeded with autologous OMECs (DL-AM+OMECs group), respectively, in a total of 54 rats (n = 18 each). Uterus samples were harvested for histological and immunohistochemical evaluation after 3, 7, 14, and 28 days (n = 3 in each time point) of operations.ResultsAfter surgery, the uterine cavity was observed to be filled with extensive fibrosis in the IUA and DL-AM groups, respectively, while a lower ratio of the fibrotic area was identified in the DL-AM transplantation group. Transplantation of OMECs seeded on DL-AM significantly reduced fibrosis of IUA with recovered uterine cavity and regenerated epithelium and endometrial glands as determined by CK-18 immunostaining. OMECs transplantation resulted in extensive cellular proliferation as revealed by the Ki-67 immunofluorescent staining exhibited. Meanwhile, microvessel density was significantly increased in uteri that received OMECs transplantation, which was concomitant with elevated expression of vascular endothelial growth factor. The pregnancy test (n = 6 in each group) showed successful conception in the OMEC-transplanted uteri, but not in the IUA and DL-AM groups.ConclusionsEngineered epithelium developed from DL-AM seeded with OMECs showed great potential in preventing progression of intrauterine adhesion by improved endometrial epithelium regeneration.Electronic supplementary materialThe online version of this article (10.1186/s13287-019-1179-z) contains supplementary material, which is available to authorized users.
In the present study, we investigated the effect of lipoxin A4 on myocardial ischemia-reperfusion injury (IRI) following cardiac arrest (CA) in a rabbit model. Lipoxin A4 is a metabolite of arachidonic acid in the eicosanoid, it is called "brake signal" for its anti-inflammatory activity. Some inflammatory factors (IL-1β, IL-6, TNF-α, and IL-10), NF-κB p65, infarct ratios, apoptotic index, cardiac troponin I (cTnI), hemodynamic and myocardial structures were measured or observed in different groups. Lipoxin A4 inhibits the expression of IL-1β, IL-6, and TNF-α, the values of the infarct ratios, apoptotic index, the level of serum cTnI and NF-κB p65. Meanwhile, it improves the expression of IL-10, hemodynamic, myocardial structure, and function. These indicate that lipoxin A4 mitigates postresuscitation myocardial IRI in which anti-inflammation and suppression of NF-κB activation may play an important role.
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