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Nosocomial coronavirus disease 2019 (COVID-19) outbreaks have been reported despite widespread quarantine methods to prevent COVID-19 in society and hospitals. Our study was performed to investigate the clinical outcome and prognosis of a nosocomial outbreak of COVID-19. We retrospectively analyzed the medical records of patients diagnosed with nosocomial COVID-19 of severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) at a university teaching hospital between 1 November 2021 and 31 April 2022. Nosocomial COVID-19 was defined as a positive SARS-CoV-2 polymerase chain reaction (PCR) test result 4 or more days after admission in asymptomatic patients who had a negative SARS-CoV-2 PCR test on admission. In this study, 167 patients were diagnosed with nosocomial COVID-19 (1.14%) among a total of 14,667 patients admitted to hospital during the study period. A total of 153 patients (91.6%) survived, but 14 patients (8.4%) died. The median time between admission and COVID-19 diagnosis was 11 days, and the median duration of hospital stay was 24 days. After adjusting for other factors, no vaccination (adjusted HR = 5.944, 95% CI = 1.626–21.733, p = 0.007) and chronic kidney disease (adjusted HR = 6.963, 95% CI = 1.182–41.014, p = 0.032) were found to increase mortality risk. Despite strict quarantine, a significant number of nosocomial COVID-19 cases with a relatively high mortality rate were reported. As unvaccinated status or chronic kidney disease were associated with poor outcomes of nosocomial COVID-19, more active preventive strategies and treatments for patients with these risk factors are needed. [ABSTRACT FROM AUTHOR]

Simple Summary: Endometriosis is a risk factor for ovarian cancer. Meta and pooled analyses have shown hormone replacement therapy (HRT) is significantly associated with an increased risk of ovarian cancer. A combination of estrogen and progesterone is currently recommended to improve menopausal symptoms in women with a history of endometriosis. However, the effect of HRT on the malignant transformation of postmenopausal endometriosis remains unclear. Therefore, this study investigated the impact of HRT on ovarian cancer occurrence in 20,608 postmenopausal women with de novo endometriosis or a history of endometriosis using the nationwide cohort study. With the exception of HRT using estrogen alone, HRT did not increase the risk of ovarian cancer in postmenopausal women with de novo endometriosis or a history of endometriosis. HRT, but not estrogen alone, can be used to improve the quality of life in symptomatic women with postmenopausal endometriosis. The effect of hormone replacement therapy (HRT) on the malignant transformation of postmenopausal endometriosis remains unclear. This study aimed to investigate the impact of HRT on ovarian cancer occurrence in postmenopausal women with de novo endometriosis or a history of endometriosis. A total of 10,304 women that received HRT (the HRT group) and 10,304 that did not (the control group) were selected by 1:1 matching those that met the study criteria. Incidences of ovarian cancer (0.3% in the HRT group and 0.5% in the control group) and cumulative incidence rates of ovarian cancer were similar in the two groups. The overall mean duration of HRT was 1.4 ± 2.2 years, but the duration of HRT in women with ovarian cancer was 2.2 ± 2.9 years. After adjusting for co-variables, receipt of HRT, duration of HRT, combined use of estrogen and progesterone, and tibolone were not found to be risk factors for ovarian cancer. However, the use of estrogen alone was found to be a significant risk factor for ovarian cancer (HR 2.898; 95% CI 1.251–6.715; p = 0.013). With the exception of HRT using estrogen alone, HRT did not increase the risk of ovarian cancer in postmenopausal women with a history of endometriosis or de novo endometriosis. [ABSTRACT FROM AUTHOR]

Vitamin C has recently been identified as an epigenetic regulator by activating ten-eleven translocases (TETs), enzymes involved in generating DNA hydroxymethylcytosine (5hmC). Currently, we investigated whether high-dose vitamin C promotes neuroprotection through epigenetic modulation of 5hmC, if there are sex-specific differences in outcome, and the therapeutic potential of vitamin C in stroke-related comorbidities in adult mice. Post-stroke treatment with ascorbate (reduced form), but not dehydroascorbate (oxidized form), increased TET3 activity and 5hmC levels and reduced infarct following focal ischemia. Hydroxymethylation DNA immunoprecipitation sequencing showed that ascorbate increased 5hmC across the genome and specifically in promoters of several stroke pathophysiology-related genes, particularly anti-inflammatory genes. Ascorbate also decreased markers of oxidative stress, mitochondrial fragmentation, and apoptosis in cortical peri-infarct neurons and promoted motor and cognitive functional recovery in both sexes via TET3. Furthermore, post-stroke ascorbate treatment reduced infarct volume and improved motor function recovery in aged, hypertensive and diabetic male and female mice. Delayed ascorbate treatment at 6 h of reperfusion was still effective at reducing infarct volume and motor impairments in adult mice. Collectively, this study shows that post-stroke treatment with high-dose ascorbate protects the brain through epigenetic reprogramming and may function as a robust therapeutic against stroke injury. [ABSTRACT FROM AUTHOR]