29 research outputs found

    The effect of cold stratification and perigynia removal on the germination of three prairie carex species

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    Sedges (Carex spp. Linneaus. [Cyperaceae]) are a major component of Midwestern U.S. tallgrass prairie and prairie wetland plant communities, yet they are often lacking in restoration projects because they can be difficult to germinate. Cold-wet stratification and perigynia removal have been shown to increase germination in some Carex species. The germination response of 3 native species, plains oval or shortbeak sedge (C. brevior (Dewey) Mack.), field oval or troublesome sedge (C. molesta Mack.), and prairie or Bicknell’s sedge (C. bicknellii Britton.), was tested to cold-wet stratification (28d) and perigynia removal in stored seed (10 months). Seed treatments included nonstratified with perigynia intact (control), nonstratified with perigynia removed, stratified with perigynia intact, and stratified with perigynia removed. Four replicates of 100 seeds treatment were held under a diurnal temperature regime 30/15 °C (86/59 °F) with 12 hours of light for 84 days. Fresh seed was also tested for C. brevior and C. molesta. Stratification increased total germination in fresh C. molesta and stored C. brevior seeds and marginal increased total germination in stored C. molesta and fresh C. bicknellii seeds. Stratification also increased germination rate in all species and seed states. Perigynia removal increased total germination in fresh C. bicknellii and stored C. brevior seeds and marginally in stored C. molesta seeds. Perigynia removal also increased germination rate in C. brevior. Combining stratification with perigynia removal did not provide any additional advantage and actually resulted in a decrease in total germination in fresh C. brevior seeds. C. molesta germinated well, to at least 91.3%, without treatment. Generally speaking, stratification overall increased germination in all species most effectively, but perigynia removal may provide some benefits if stratification is not available

    The Association of Childhood Maltreatment With Lipid Peroxidation and DNA Damage in Postpartum Women

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    Childhood maltreatment (CM) is associated with an increased risk for the development of psychiatric and somatic disorders in later life. A potential link could be oxidative stress, which is defined as the imbalance between the amount of reactive oxygen species (ROS) and the neutralizing capacity of anti-oxidative defense systems. However, the findings linking CM with oxidative stress have been inconsistent so far. In this study, we aimed to further explore this association by investigating biological markers of DNA and lipid damage due to oxidation in a comprehensive approach over two study cohorts of postpartum women (study cohort I and study cohort II). The severity of CM experiences (maltreatment load) was assessed in both studies using the Childhood Trauma Questionnaire. In study cohort I (N = 30), we investigated whether CM was associated with higher levels of structural DNA damage in peripheral blood mononuclear cells (PBMC) by two methods that are highly sensitive for detecting nuclear DNA strand breaks (comet assay and γH2AX staining). In study cohort II (N = 117), we then assessed in a larger cohort, that was specifically controlled for potential confounders for oxidative stress measurements, two established serum and plasma biomarkers of oxidative stress, one representing oxidative DNA and RNA damage (8-hydroxy-2′-deoxyguanosine and 8-hydroxyguanosine; 8-OH(d)G) and the other representing lipid peroxidation (8-isoprostane). In study cohort I, the analyses revealed no significant main effects of maltreatment load on cellular measures of nuclear DNA damage. The analyses of peripheral oxidative stress biomarkers in study cohort II revealed a significant main effect of maltreatment load on free 8-isoprostane plasma levels, but not on total 8-isprostane plasma levels and 8-OH(d)G serum levels. Taken together, by combining different methods and two study cohorts, we found no indications for higher oxidative DNA damages with higher maltreatment load in postpartum women. Further research is needed to investigate whether this increase in free 8-isoprostane is a marker for oxidative stress or whether it is instead functionally involved in ROS-related signaling pathways that potentially regulate inflammatory processes following a history of CM

    Impact of COVID-19 on cardiovascular testing in the United States versus the rest of the world

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    Objectives: This study sought to quantify and compare the decline in volumes of cardiovascular procedures between the United States and non-US institutions during the early phase of the coronavirus disease-2019 (COVID-19) pandemic. Background: The COVID-19 pandemic has disrupted the care of many non-COVID-19 illnesses. Reductions in diagnostic cardiovascular testing around the world have led to concerns over the implications of reduced testing for cardiovascular disease (CVD) morbidity and mortality. Methods: Data were submitted to the INCAPS-COVID (International Atomic Energy Agency Non-Invasive Cardiology Protocols Study of COVID-19), a multinational registry comprising 909 institutions in 108 countries (including 155 facilities in 40 U.S. states), assessing the impact of the COVID-19 pandemic on volumes of diagnostic cardiovascular procedures. Data were obtained for April 2020 and compared with volumes of baseline procedures from March 2019. We compared laboratory characteristics, practices, and procedure volumes between U.S. and non-U.S. facilities and between U.S. geographic regions and identified factors associated with volume reduction in the United States. Results: Reductions in the volumes of procedures in the United States were similar to those in non-U.S. facilities (68% vs. 63%, respectively; p = 0.237), although U.S. facilities reported greater reductions in invasive coronary angiography (69% vs. 53%, respectively; p < 0.001). Significantly more U.S. facilities reported increased use of telehealth and patient screening measures than non-U.S. facilities, such as temperature checks, symptom screenings, and COVID-19 testing. Reductions in volumes of procedures differed between U.S. regions, with larger declines observed in the Northeast (76%) and Midwest (74%) than in the South (62%) and West (44%). Prevalence of COVID-19, staff redeployments, outpatient centers, and urban centers were associated with greater reductions in volume in U.S. facilities in a multivariable analysis. Conclusions: We observed marked reductions in U.S. cardiovascular testing in the early phase of the pandemic and significant variability between U.S. regions. The association between reductions of volumes and COVID-19 prevalence in the United States highlighted the need for proactive efforts to maintain access to cardiovascular testing in areas most affected by outbreaks of COVID-19 infection

    Werknemersreacties op (exclusief) talentmanagement

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    Progression of arteriovenous bypass restenosis in mice exposed to a 50 Hz magnetic field

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    The controversy over whether magnetic fields (MF) produced by electrical wiring and appliances contribute to diseases such as cancer has been debated in the literature for more than 2 decades. These extremely low frequency fields at 50 or 60 Hz are omnipresent in the industrialized world and have been linked to various forms of cancer by epidemiological studies. Little has been published investigating any possible role of MF and cardiovascular disease, and this is the first study looking specifically at the effect of exposure to high-intensity MF on the development and progression of restenosis. A mouse arteriovenous bypass model was used, and mice were exposed to MF for periods of 1, 2, or 3 weeks. Neointima formation, infiltration of mononuclear cells, and heat shock protein 60 expression were all studied at the conclusion of the exposure regimen. Animals exposed to the MF for 1 week showed significantly smaller neointima formation compared with control mice exposed to a null field, although this difference was not observed in mice exposed for 2 or 3 weeks. No difference was found between mice exposed to MF and controls in any of the other parameters investigated

    Investigating the effects of childhood maltreatment on pro-inflammatory signaling:The influence of cortisol and DHEA on cytokine secretion ex vivo

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    Childhood maltreatment (CM) is associated with chronic low-grade inflammation and an increased risk for the development of adverse mental and physical health outcomes in CM-affected adults. Differences in cortisol signaling were described to contribute to this pro-inflammatory phenotype. We investigated in a study cohort of 13 postpartum women with and 12 postpartum women without CM whether treatment of peripheral blood mononuclear cells (PBMC) with cortisol, the anti-glucocorticoid hormone dehydroepiandrosterone (DHEA), or co-treatment with both differentially affected pro-inflammatory cytokine release ex vivo. The childhood trauma questionnaire was used to retrospectively assess CM and the severity of CM experiences (maltreatment load). PBMC of maltreated women (CM+) showed in all conditions an increase in pro-inflammatory cytokine secretion compared to PBMC of the control group (CM-), which was correlated with the maltreatment load. Ex vivo stimulation analyses provided preliminary evidence for a differential responsivity of PBMC in CM+ and CM- women to cortisol regarding TNF-α secretion, but no difference in the responsivity to DHEA treatment. The results of the co-treatment with cortisol and DHEA support the hypothesis that cortisol and DHEA interact in the modulation of inflammatory processes

    Associations between childhood maltreatment and DNA methylation of the oxytocin receptor gene in immune cells of mother–newborn dyads

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    The neuropeptide oxytocin (OXT) and its receptor (OXTR) modulate interpersonal relationships, particularly mother-child interactions. DNA methylation (DNAm) changes of the OXTR gene were observed in individuals who experienced Childhood Maltreatment (CM). A modulatory role of single nucleotide polymorphisms (SNP) within OXTR in association with CM on the regulation of OXTR was also postulated. Whether these CM-induced epigenetic alterations are biologically inherited by the offspring remains unknown. We thus investigated possible intergenerational effects of maternal CM exposure on DNAm and OXTR gene expression, additionally accounting for the possible influence of three SNP: rs53576 and rs2254298 (OXTR gene), and rs2740210 (OXT gene). We used the Childhood Trauma Questionnaire to classify mothers into individuals with (CM+) or without CM (CM-). Maternal peripheral immune cells were isolated from venous blood (N = 117) and fetal immune cells from the umbilical cord (N = 113) after parturition. DNA methylation was assessed using MassARRAY. Taqman assays were performed for genotyping and gene expression analyses. Among mothers, CM was not associated with OXTR mean methylation or gene expression. However, four CpG sites showed different methylation levels in CM- compared to CM+. In mothers, the OXTR rs53576 and OXT rs2740210 allelic variations interacted with CM load on the OXTR mean methylation. Maternal and newborns' mean methylation of OXTR were positively associated within CM- dyads, but not in CM+ dyads. We show genexenvironment interactions on the epigenetic regulation of the oxytocinergic signaling and show the intergenerational comparability of the OXTR DNAm might be altered in infants of CM+ mothers

    Alterations of the serum N-glycan profile in female patients with Major Depressive Disorder

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    Background: Glycans are short chains of saccharides linked to glycoproteins that are known to be involved in a wide range of inflammatory processes. As depression has been consistently associated with chronic low-grade inflammation, we asked whether patients with Major Depressive Disorder show alterations in the N-glycosylation pattern of serum proteins that might be linked to associated changes in inflammatory processes. Methods: In a study cohort of 21 female patients with an acute depressive episode and 21 non-depressed female control subjects aged between 50 and 69 years, we analyzed the serum N-glycan profile by DNA Sequencer Adapted-Fluorophore Assisted Carbohydrate Electrophoresis (DSA-FACE) and assessed the serum levels of interleukin (IL)-6, tumor necrosis factor (TNF)-alpha and C-reactive protein (CRP) by chemiluminescence immunoassays and nephelometry. Results: Compared to controls, MDD patients showed significant differences in the serum levels of several N-glycan structures. Alterations in the serum N-glycan profile were associated with depressive symptom severity and exploratory analyses revealed that they were most pronounced in MDD patients with a history of childhood sexual abuse. Furthermore, MDD patients showed higher levels of IL-6 and a trend for higher CRP levels, which were also associated with similar alterations in the serum N-glycan profile as those characteristic for MDD patients. Limitations: The relatively small sample size and the presence of potential confounders (e.g., BMI, smoking, medication). Conclusion: The results offer the first evidence that specific differences in the N-glycosylation pattern of serum proteins constitute a so far unrecognized level of biological alterations that might be involved in the immune changes associated with MDD
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