332 research outputs found

    Rates of depressive and anxiety symptoms in the perinatal period during the COVID-19 pandemic: Comparisons between countries and with pre-pandemic data

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    Background: The COVID-19 pandemic was a significant threat to perinatal mental health. This study examined differences in clinically significant depression, anxiety, and co-morbid symptoms among pregnant and postpartum women across several countries and compared prevalence of perinatal depression and anxiety before and during the pandemic in each participating country. Methods: Participants were 3326 pregnant and 3939 postpartum women (up to six months postpartum) living in Brazil, Chile, Cyprus, Greece, Israel, Portugal, Spain, Turkey, and the United Kingdom. An online survey was completed between June 7th and October 31st 2020, and included the Edinburgh Postnatal Depression Scale (EPDS) and the Generalized Anxiety Disorder Screener (GAD-7). The pre-pandemic studies were identified through literature review. Results: Prevalence of clinically significant depression (EPDS≥13), anxiety (GAD-7 ≥ 10), and co-morbid (EPDS≥13 and GAD-7 ≥ 10) symptoms was 26.7 %, 20 % and 15.2 %, in pregnant women, and 32.7 %, 26.6 % and 20.3 %, in postpartum women, respectively. Significant between-country differences were found in all mental health indicators in both perinatal periods. Higher levels of symptoms were observed during (versus before) the pandemic, especially among postpartum women. Limitations: Participants were mostly highly educated and cohabiting with a partner. The online nature of the survey may have limited the participation of women from vulnerable socio-economically backgrounds. Conclusions: Our findings expand previous literature on the negative impact of the COVID-19 pandemic on perinatal mental health, by highlighting that this may be influenced by country of residence. Mental health care policies and interventions should consider the unique needs of perinatal women in different parts of the world. © 2022Funding text 1: Sara Cruz acknowledges the Centro de Investigação em Psicologia para o Desenvolvimento (CIPD) [The Psychology for Positive Development Research Center] ( UID/PSI/04375 ), Lusíada University North, Porto, supported by national funds through the Portuguese Foundation for Science and Technology , I.P., and the Portuguese Ministry of Science, Technology and Higher Education ( UID/PSI/04375/2019 ).; Funding text 2: This paper is part of the COST Action Riseup-PPD CA18138 and was supported by COST under COST Action Riseup-PPD CA18138 . ; Funding text 3: Vera Mateus received financial support from CAPES /PrInt grant no. 88887.583508/2020-00 . ; Funding text 4: Raquel Costa was supported by the FSE and FCT under the Post-Doctoral Grant SFRH/BPD/117597/2016 [RC]. EPIUnit, ITR, and HEI-lab are supported by national funds through the Portuguese Foundation for Science and Technology , I.P., under the projects UIDB/04750/2020 , LA/P/0064/2020 , and UIDB/05380/2020 , respectively. ; Funding text 5: This publication is based upon work from COST Action 18138 - Research Innovation and Sustainable Pan-European Network in Peripartum Depression Disorder (Riseup-PPD), supported by COST (European Cooperation in Science and Technology). www.cost.eu . ; Funding text 6: Ana Osório received financial support from CAPES PROEX grant no. 0426/2021 , process no. 23038.006837/2021-73, CAPES /PrInt grant no. 88887.310343/2018-00 and MackPesquisa Fund . ; Funding text 7: Rena Bina received financial support from the Bar-Ilan Dangoor Centre for Personalized Medicine , grant no. REFU/DANGO/100. ; Funding text 8: This publication is based upon work from COST Action 18138 - Research Innovation and Sustainable Pan-European Network in Peripartum Depression Disorder (Riseup-PPD), supported by COST (European Cooperation in Science and Technology). www.cost.eu.Vera Mateus received financial support from CAPES/PrInt grant no. 88887.583508/2020-00.Ana Osório received financial support from CAPES PROEX grant no. 0426/2021, process no. 23038.006837/2021-73, CAPES/PrInt grant no. 88887.310343/2018-00 and MackPesquisa Fund.Rena Bina received financial support from the Bar-Ilan Dangoor Centre for Personalized Medicine, grant no. REFU/DANGO/100.Raquel Costa was supported by the FSE and FCT under the Post-Doctoral Grant SFRH/BPD/117597/2016 [RC]. EPIUnit, ITR, and HEI-lab are supported by national funds through the Portuguese Foundation for Science and Technology, I.P., under the projects UIDB/04750/2020, LA/P/0064/2020, and UIDB/05380/2020, respectively.This paper is part of the COST Action Riseup-PPD CA18138 and was supported by COST under COST Action Riseup-PPD CA18138. The authors would like to thank all women who participated in the survey. Sara Cruz acknowledges the Centro de Investigação em Psicologia para o Desenvolvimento (CIPD) [The Psychology for Positive Development Research Center] (UID/PSI/04375), Lusíada University North, Porto, supported by national funds through the Portuguese Foundation for Science and Technology, I.P. and the Portuguese Ministry of Science, Technology and Higher Education (UID/PSI/04375/2019)

    Cellular Angiofibroma of Oral Mucosa: Report of Two Cases

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    Cellular angiofibroma is a benign vascular neoplasm that typically arises in the vulva, perineal, and paratesticular region. Microscopically the lesions exhibit multiple small, non-dilated capillary channels, many of which contain erythrocytes. The endothelial lining cells are prominent, with monomorphic oval nuclei. Interposed among the vessels are both delicate and mature collagen fibers with fibroblastic hypercellularity that is variable in older lesions where sclerosis is prominent. The lesions usually do not recur following simple excision. Recent evidence indicates that cellular angiofibromas may be cytogenetically related to spindle cell lipoma. This represents the first reported instances of cellular angiofibroma in the oral cavity

    Impact of the Covid-19 pandemic on perinatal mental health (Riseup-PPD-COVID-19): protocol for an international prospective cohort study

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    Background: Corona Virus Disease 19 (COVID-19) is a new pandemic, declared a public health emergency by the World Health Organization, which could have negative consequences for pregnant and postpartum women. The scarce evidence published to date suggests that perinatal mental health has deteriorated since the COVID-19 outbreak. However, the few studies published so far have some limitations, such as a cross-sectional design and the omission of important factors for the understanding of perinatal mental health, including governmental restriction measures and healthcare practices implemented at the maternity hospitals. Within the Riseup-PPD COST Action, a study is underway to assess the impact of COVID-19 in perinatal mental health. The primary objectives are to (1) evaluate changes in perinatal mental health outcomes; and (2) determine the risk and protective factors for perinatal mental health during the COVID-19 pandemic. Additionally, we will compare the results between the countries participating in the study. Methods: This is an international prospective cohort study, with a baseline and three follow-up assessments over a six-month period. It is being carried out in 11 European countries (Albania, Bulgaria, Cyprus, France, Greece, Israel, Malta, Portugal, Spain, Turkey, and the United Kingdom), Argentina, Brazil and Chile. The sample consists of adult pregnant and postpartum women (with infants up to 6 months of age). The assessment includes measures on COVID-19 epidemiology and public health measures (Oxford COVID-19 Government Response Tracker dataset), Coronavirus Perinatal Experiences (COPE questionnaires), psychological distress (BSI-18), depression (EPDS), anxiety (GAD-7) and post-traumatic stress symptoms (PTSD checklist for DSM-V). Discussion: This study will provide important information for understanding the impact of the COVID-19 pandemic on perinatal mental health and well-being, including the identification of potential risk and protective factors by implementing predictive models using machine learning techniques. The findings will help policymakers develop suitable guidelines and prevention strategies for perinatal mental health and contribute to designing tailored mental health interventions. Trial registration: ClinicalTrials.gov Identifier: NCT04595123.The project is part of the COST Action Riseup-PPD CA 18138 and was supported by COST under COST Action Riseup-PPD CA18138; also, by the Spanish Ministry of Health, the Institute of Health Carlos III, and the European Regional Development Fund «Una manera de hacer Europa» by the Prevention and Health Promotion Research Network ‘redIAPP’ (RD16/0007). Raquel Costa is supported by the FSE and FCT under an individual Post-Doctoral Grant SFRH/BPD/117597/2016. Rena Bina and Drorit Levy received funding from the Bar-Ilan Dangoor Centre for Personalized Medicine, Israel. Ana Mesquita is supported from the Portuguese Foundation for Science and Technology (FCT) and from EU through the European Social Fund and from the Human Potential Operational Program - IF/00750/2015. Ana Osório received financial support from CAPES/Proex no. 0653/2018 and CAPES/PrInt grant no. 88887.310343/2018-00.The funders of the study had no role in the study design or the writing the protocol. The corresponding author had final responsibility for the decision to submit for publication

    Bicyclic triterpenoid Iripallidal induces apoptosis and inhibits Akt/mTOR pathway in glioma cells

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    <p>Abstract</p> <p>Background</p> <p>The highly resistant nature of glioblastoma multiforme (GBM) to chemotherapy prompted us to evaluate the efficacy of bicyclic triterpenoid Iripallidal against GBM in vitro.</p> <p>Methods</p> <p>The effect of Iripallidal on proliferation and apoptosis in glioma cell lines was evaluated by MTS, colony formation and caspase-3 activity. The effect of iripallidal to regulate (i) Akt/mTOR and STAT3 signaling (ii) molecules associated with cell cycle and DNA damage was evaluated by Western blot analysis. The effect of Iripallidal on telomerase activity was also determined.</p> <p>Results</p> <p>Iripallidal (i) induced apoptosis, (ii) inhibited Akt/mTOR and STAT3 signaling, (iii) altered molecules associated with cell cycle and DNA damage, (iv) inhibited telomerase activity and colony forming efficiency of glioma cells. In addition, Iripallidal displayed anti-proliferative activity against non-glioma cancer cell lines of diverse origin.</p> <p>Conclusion</p> <p>The ability of Iripallidal to serve as a dual-inhibitor of Akt/mTOR and STAT3 signaling warrants further investigation into its role as a therapeutic strategy against GBM.</p

    RHPS4 G-quadruplex ligand induces anti-proliferative effects in brain tumor cells

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    Background Telomeric 3’ overhangs can fold into a four-stranded DNA structure termed G-quadruplex (G4), a formation which inhibits telomerase. As telomerase activation is crucial for telomere maintenance in most cancer cells, several classes of G4 ligands have been designed to directly disrupt telomeric structure. Methods We exposed brain tumor cells to the G4 ligand 3,11-difluoro-6,8,13-trimethyl-8H-quino[4,3,2-kl]acridinium methosulfate (RHPS4) and investigated proliferation, cell cycle dynamics, telomere length, telomerase activity and activated c-Myc levels. Results Although all cell lines tested were sensitive to RHPS4, PFSK-1 central nervous system primitive neuroectodermal cells, DAOY medulloblastoma cells and U87 glioblastoma cells exhibited up to 30-fold increased sensitivity compared to KNS42 glioblastoma, C6 glioma and Res196 ependymoma cells. An increased proportion of S-phase cells were observed in medulloblastoma and high grade glioma cells whilst CNS PNET cells showed an increased proportion of G1-phase cells. RHPS4-induced phenotypes were concomitant with telomerase inhibition, manifested in a telomere length-independent manner and not associated with activated c-Myc levels. However, anti-proliferative effects were also observed in normal neural/endothelial cells in vitro and ex vivo. Conclusion This study warrants in vivo validation of RHPS4 and alternative G4 ligands as potential anti-cancer agents for brain tumors but highlights the consideration of dose-limiting tissue toxicities

    Telomerase Inhibition Targets Clonogenic Multiple Myeloma Cells through Telomere Length-Dependent and Independent Mechanisms

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    Plasma cells constitute the majority of tumor cells in multiple myeloma (MM) but lack the potential for sustained clonogenic growth. In contrast, clonotypic B cells can engraft and recapitulate disease in immunodeficient mice suggesting they serve as the MM cancer stem cell (CSC). These tumor initiating B cells also share functional features with normal stem cells such as drug resistance and self-renewal potential. Therefore, the cellular processes that regulate normal stem cells may serve as therapeutic targets in MM. Telomerase activity is required for the maintenance of normal adult stem cells, and we examined the activity of the telomerase inhibitor imetelstat against MM CSC. Moreover, we carried out both long and short-term inhibition studies to examine telomere length-dependent and independent activities.Human MM CSC were isolated from cell lines and primary clinical specimens and treated with imetelstat, a specific inhibitor of the reverse transcriptase activity of telomerase. Two weeks of exposure to imetelstat resulted in a significant reduction in telomere length and the inhibition of clonogenic MM growth both in vitro and in vivo. In addition to these relatively long-term effects, 72 hours of imetelstat treatment inhibited clonogenic growth that was associated with MM CSC differentiation based on expression of the plasma cell antigen CD138 and the stem cell marker aldehyde dehydrogenase. Short-term treatment of MM CSC also decreased the expression of genes typically expressed by stem cells (OCT3/4, SOX2, NANOG, and BMI1) as revealed by quantitative real-time PCR.Telomerase activity regulates the clonogenic growth of MM CSC. Moreover, reductions in MM growth following both long and short-term telomerase inhibition suggest that it impacts CSC through telomere length-dependent and independent mechanisms
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