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( Camila Oliveira Serra ),( Paula Mara Gomes Leite ),( Andráa Beatriz Bezerra ),( Laura Freitas ),( Lucas Veras ),( Marcela Deda Costa ),( Leila Luiza Conceição Gonçalves ),( Leonardo Yung Dos Santos 대한폐경학회 2022 대한폐경학회지 Vol.28 No.1
Objectives: This study aimed to compare the climacteric symptoms, quality of life indices, and self-care attitudes in women before and during the coronavirus disease 2019 (COVID-19) pandemic. Methods: This cross-sectional study was conducted between January 2020 and September 2021. The sample consisted of 342 climacteric women who were divided into two groups: before the pandemic (BP group; n = 62) and during the pandemic (DP group; n = 280). The Menopause Rating Scale and Women’s Health Questionnaire were used to measure the health-related quality of life and degree of climacteric symptoms reported by women. Results: During the COVID-19 pandemic, women were able to decrease their somatic symptoms derived from the climacteric period (BP group: 7.84 ± 4.46, DP group: 5.94 ± 9.20; P = 0.003). Conclusions: There was no worsening in the self-reported symptoms, quality of life, and self-care attitudes of climacteric women because of the COVID-19 pandemic. Moreover, only somatic symptoms decreased during the pandemic.
Recurrent <i>ETNK1</i> mutations in atypical chronic myeloid leukemia
Gambacorti-Passerini, Carlo B.,Donadoni, Carla,Parmiani, Andrea,Pirola, Alessandra,Redaelli, Sara,Signore, Giovanni,Piazza, Vincenzo,Malcovati, Luca,Fontana, Diletta,Spinelli, Roberta,Magistroni, Vera American Society of Hematology 2015 Blood Vol.125 No.3
<P>Despite the recent identification of recurrent <I>SETBP1</I> mutations in atypical chronic myeloid leukemia (aCML), a complete description of the somatic lesions responsible for the onset of this disorder is still lacking. To find additional somatic abnormalities in aCML, we performed whole-exome sequencing on 15 aCML cases. In 2 cases (13.3%), we identified somatic missense mutations in the <I>ETNK1</I> gene. Targeted resequencing on 515 hematological clonal disorders revealed the presence of <I>ETNK1</I> variants in 6 (8.8%) of 68 aCML and 2 (2.6%) of 77 chronic myelomonocytic leukemia samples. These mutations clustered in a small region of the kinase domain, encoding for H243Y and N244S (1/8 H243Y; 7/8 N244S). They were all heterozygous and present in the dominant clone. The intracellular phosphoethanolamine/phosphocholine ratio was, on average, 5.2-fold lower in ETNK1-mutated samples (<I>P</I> < .05). Similar results were obtained using myeloid TF1 cells transduced with ETNK1 wild type, ETNK1-N244S, and ETNK1-H243Y, where the intracellular phosphoethanolamine/phosphocholine ratio was significantly lower in ETNK1-N244S (0.76 ± 0.07) and ETNK1-H243Y (0.37 ± 0.02) than in ETNK1-WT (1.37 ± 0.32; <I>P</I> = .01 and <I>P</I> = .0008, respectively), suggesting that <I>ETNK1</I> mutations may inhibit the catalytic activity of the enzyme. In summary, our study shows for the first time the evidence of recurrent somatic <I>ETNK1</I> mutations in the context of myeloproliferative/myelodysplastic disorders.</P>