Browsing by Author "Gutierrez, Jorge"
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- ItemIncrease in maternal mortality and prematurity during the COVID-19 pandemic in Chile(2023) Gonzalez, Rogelio; Viviani, Paola; Merialdi, Mario; Rubio, Gonzalo; Pons, Andres; Gutierrez, JorgeIntroduction: At the third year of the pandemic in Chile, the reported cases of COVID-19 reached 4,769,638 and 61,725 deaths (1.4%), with 93% of the population with a complete vaccination schedule (17,686,528). Aim: The purpose of this study is a brief communication on the impact of the SARS-CoV-2 pandemic on maternal, perinatal and prematurity mortality in Chile. Method: The national database of the Informatics Department of the Ministry of Health of Chile (DEIS), and the information reported from the official WHO website were used. All births, general and fetal deaths from January 1990 to September 2022 were included. A comparison is made between the basic maternal and perinatal indicators of the last 30 years and those of the years of the pandemic. Results: From March 2020 to September 2022, approximately 61,000 people died in Chile with a diagnosis associated with COVID-19, 17% of the general mortality for the period (approx. 364.000 deaths). An acceleration in the historical trend towards a decrease in the overall birth/death ratio was observed from 1.9 pre-pandemic to 1.4 during the third year of the pandemic. Maternal Mortality Ratio in 2020 (28.1 x 100,000) increased compared to 2019 pre-pandemic (19.1) or the simple historical trend line projected for 2020 (18.0) by 56%. Prematurity under 37 weeks of gestation increased from 8.5% (2019) to 9.5% for the years 2021 and 2022. Neonatal mortality in the first 28 days remained stable at 9 per thousand births during the 3 years of the pandemic and fetal mortality (>21 weeks) had a slight increase to 4.7 per thousand (year 2020) in relation to 3.4 in 2019. Conclusions: In Chile, an increase of approximately 56% in maternal mortality occurred in the first year of the SARS-CoV-2 pandemic. In the second year, a significant increase in late prematurity and a slight increase in fetal mortality were observed. These findings have been reported in the reviews and latest updates of the year 2022.
- ItemProgesterone Utilizes Distinct Membrane Pools of Tissue Factor to Increase Coagulation and Invasion and These Effects are Inhibited by TFPI(WILEY, 2011) Henriquez, Soledad; Calderon, Claudia; Quezada, Marisol; Oliva, Barbara; Loreto Bravo, Maria; Aranda, Evelyn; Kato, Sumie; Cuello, Mauricio A.; Gutierrez, Jorge; Quest, Andrew F. G.; Owen, Gareth I.Tissue factor (TF) serving as the receptor for coagulation factor VII (FVII) initiates the extrinsic coagulation pathway. We previously demonstrated that progesterone increases TF, coagulation and invasion in breast cancer cell lines. Herein, we investigated if tissue factor pathway inhibitor (TFPI) could down-regulate progesterone-increased TF activity in these cells. Classically, TFPI redistributes TF-FVII-FX-TFPI in an inactive quaternary complex to membrane associated lipid raft regions. Herein, we demonstrate that TF increased by progesterone is localized to the heavy membrane fraction, despite progesterone-increased coagulation originating almost exclusively from lipid raft domains, where TF levels are extremely low. The progesterone increase in coagulation is not a rapid effect, but is progesterone receptor (PR) dependent and requires protein synthesis. Although a partial relocalization of TF occurs, TFPI does not require the redistribution to lipid rafts to inhibit coagulation or invasion. Inhibition by TFPI and anti-TF antibodies in lipid raft membrane fractions confirmed the dependence on TF for progesterone-mediated coagulation. Through the use of pathway inhibitors, we further demonstrate that the TF up-regulated by progesterone is not coupled to the progesterone increase in TF-mediated coagulation. However, the progesterone up-regulated TF protein may be involved in progesterone-mediated breast cancer cell invasion, which TFPI also inhibits. J. Cell. Physiol. 226: 3278-3285, 2011. (C) 2011 Wiley Periodicals, Inc.