| 1. |
- Bernal, Ximena E., et al.
(författare)
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Empowering Latina scientists
- 2019
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 363:6429, s. 825-826
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 2. |
- Dagher, Rada K., et al.
(författare)
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Postpartum depressive symptoms and the combined load of paid and unpaid work : a longitudinal analysis
- 2011
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Ingår i: International Archives of Occupational and Environmental Health. - : Springer. - 0340-0131 .- 1432-1246. ; 84:7, s. 735-743
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Tidskriftsartikel (refereegranskat)abstract
- Purpose: To investigate the effects of total workload and other work-related factors on postpartum depression in the first 6 months after childbirth, utilizing a hybrid model of health and workforce participation. Methods: We utilized data from the Maternal Postpartum Health Study collected in 2001 from a prospective cohort of 817 employed women who delivered in three commu- nity hospitals in Minnesota. Interviewers collected data at enrollment and 5 weeks, 11 weeks, and 6 months after childbirth. The Edinburgh Postnatal Depression Scale measured postpartum depression. Independent variables included total workload (paid and unpaid work), job flex- ibility, supervisor and coworker support, available social support, job satisfaction, infant sleep problems, infant irritable temperament, and breastfeeding. Results: Total average daily workload increased from 14.4 h (6.8 h of paid work; 7.1% working at 5 weeks postpartum) to 15.0 h (7.9 h of paid work; 87% working at 6 months postpartum) over the 6 months. Fixed effects regression analyses showed worse depression scores were associated with higher total workload, lower job flexibility, lower social support, an infant with sleep problems, and breastfeeding. Conclusions: Working mothers of reproductive years may find the study results valuable as they consider merging their work and parenting roles after childbirth. Future studies should examine the specific mechanisms through which total workload affects postpartum depressive symptoms.
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| 3. |
- Ferreira, Vitor, et al.
(författare)
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Modulation of hypothalamic AMPK phosphorylation by olanzapine controls energy balance and body weight
- 2022
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Ingår i: Metabolism. - : Elsevier. - 0026-0495 .- 1532-8600. ; 137
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Tidskriftsartikel (refereegranskat)abstract
- Background: Second-generation antipsychotics (SGAs) are a mainstay therapy for schizophrenia. SGA-treated patients present higher risk for weight gain, dyslipidemia and hyperglycemia. Herein, we evaluated the effects of olanzapine (OLA), widely prescribed SGA, in mice focusing on changes in body weight and energy balance. We further explored OLA effects in protein tyrosine phosphatase-1B deficient (PTP1B-KO) mice, a preclinical model of leptin hypersensitivity protected against obesity. Methods: Wild-type (WT) and PTP1B-KO mice were fed an OLA-supplemented diet (5 mg/kg/day, 7 months) or treated with OLA via intraperitoneal (i.p.) injection or by oral gavage (10 mg/kg/day, 8 weeks). Readouts of the crosstalk between hypothalamus and brown or subcutaneous white adipose tissue (BAT and iWAT, respectively) were assessed. The effects of intrahypothalamic administration of OLA with adenoviruses expressing constitutive active AMPK alpha 1 in mice were also analyzed. Results: Both WT and PTP1B-KO mice receiving OLA-supplemented diet presented hyperphagia, but weight gain was enhanced only in WT mice. Unexpectedly, all mice receiving OLA via i.p. lost weight without changes in food intake, but with increased energy expenditure (EE). In these mice, reduced hypothalamic AMPK phosphorylation concurred with elevations in UCP-1 and temperature in BAT. These effects were also found by intrahypothalamic OLA injection and were abolished by constitutive activation of AMPK in the hypothalamus. Additionally, OLA i. p. treatment was associated with enhanced Tyrosine Hydroxylase (TH)-positive innervation and less sympathetic neuron-associated macrophages in iWAT. Both central and i.p. OLA injections increased UCP-1 and TH in iWAT, an effect also prevented by hypothalamic AMPK activation. By contrast, in mice fed an OLA-supplemented diet, BAT thermogenesis was only enhanced in those lacking PTP1B. Our results shed light for the first time that a threshold of OLA levels reaching the hypothalamus is required to activate the hypothalamus BAT/iWAT axis and, therefore, avoid weight gain. Conclusion: Our results have unraveled an unexpected metabolic rewiring controlled by hypothalamic AMPK that avoids weight gain in male mice treated i.p. with OLA by activating BAT thermogenesis and iWAT browning and a potential benefit of PTP1B inhibition against OLA-induced weight gain upon oral treatment.
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| 4. |
- McGovern, Patricia, et al.
(författare)
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A Longitudinal Analysis of Total Workload and Women's Health After Childbirth
- 2011
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Ingår i: Journal of Occupational and Environmental Medicine. - : Wolters Kluwer. - 1076-2752 .- 1536-5948. ; 53:5, s. 497-505
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Tidskriftsartikel (refereegranskat)abstract
- Objectives: To examine the association of women's postpartum health with total workload (TWL), work and personal factors in the year after childbirth. Methods: Employed women from Minneapolis and St Paul, Minnesota, were recruited while hospitalized for childbirth. Longitudinal analyses, using fixed effects regression models, estimated the associations of TWL, job satisfaction and stress, social support, perceived control, breastfeeding and infant characteristics with women's health at 5 weeks, 11 weeks, 6 months, and 12 months postpartum. Results: Increased TWL over time was associated with significantly poorer mental health and increased symptoms. Conclusions: High TWL-including reduced time for rest, recovery, and sleep-is a risk factor for women's mental health and symptoms 12 months after childbirth. Women's postpartum health was positively associated with social support, which may help to decrease the negative effects of excess work.
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| 5. |
- Rada-Iglesias, Alvaro, et al.
(författare)
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Butyrate mediates decrease of histone acetylation centered on transcription start sites and down-regulation of associated genes
- 2007
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Ingår i: Genome Research. - : Cold Spring Harbor Laboratory. - 1088-9051 .- 1549-5469. ; 17:6, s. 708-719
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Tidskriftsartikel (refereegranskat)abstract
- Butyrate is a histone deacetylase inhibitor (HDACi) with anti-neoplastic properties, which theoretically reactivates epigenetically silenced genes by increasing global histone acetylation. However, recent studies indicate that a similar number or even more genes are down-regulated than up-regulated by this drug. We treated hepatocarcinoma HepG2 cells with butyrate and characterized the levels of acetylation at DNA-bound histones H3 and H4 by ChIP-chip along the ENCODE regions. In contrast to the global increases of histone acetylation, many genomic regions close to transcription start sites were deacetylated after butyrate exposure. In order to validate these findings, we found that both butyrate and trichostatin A treatment resulted in histone deacetylation at selected regions, while nucleosome loss or changes in histone H3 lysine 4 trimethylation (H3K4me3) did not occur in such locations. Furthermore, similar histone deacetylation events were observed when colon adenocarcinoma HT-29 cells were treated with butyrate. In addition, genes with deacetylated promoters were down-regulated by butyrate, and this was mediated at the transcriptional level by affecting RNA polymerase II (POLR2A) initiation/elongation. Finally, the global increase in acetylated histones was preferentially localized to the nuclear periphery, indicating that it might not be associated to euchromatin. Our results are significant for the evaluation of HDACi as anti-tumourogenic drugs, suggesting that previous models of action might need to be revised, and provides an explanation for the frequently observed repression of many genes during HDACi treatment.
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| 6. |
- Respuela, Patricia, 1977-, et al.
(författare)
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Histone acetylation and methylation at sites initiating divergent polycistronic transcription in Trypanosoma cruzi
- 2008
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Ingår i: Journal of Biological Chemistry. - 0021-9258 .- 1083-351X. ; 283:23, s. 15884-15892
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Tidskriftsartikel (refereegranskat)abstract
- Trypanosomes are ancient eukaryotic parasites in which the protein-coding genes, organized in large polycistronic clusters on both strands, are transcribed from as yet unidentified promoters. In an effort to reveal transcriptional initiation sites, we examined the Trypanosoma cruzi genome for histone modification patterns shown to be linked to active genes in various organisms. Here, we show that acetylated and methylated histones were found to be enriched at strand switch regions of divergent gene arrays, not at convergent clusters or intra- and intergenic regions within clusters. The modified region showed a bimodular profile with two peaks centered over the 5'-regions of the gene pair flanking the strand switch region. This pattern, which demarcates polycistronic transcription units originating from bidirectional initiation sites, is likely to be common in kinetoplastid parasites as well as in other organisms with polycistronic transcription. In contrast, no acetylation was found at promoters of the highly expressed rRNA and spliced leader genes or satellite DNA or at tested retrotransposonal elements. These results reveal, for the first time, the presence of specific epigenetic marks in T. cruzi with potential implications for transcriptional regulation; they indicate that both histone modifications and bidirectional transcription are evolutionarily conserved.
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