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  • 1
    Publication Date: 2018-07-28
    Description: A user-friendly herbicide derived from photo-responsive supramolecular vesicles A user-friendly herbicide derived from photo-responsive supramolecular vesicles, Published online: 27 July 2018; doi:10.1038/s41467-018-05437-5 Paraquat is a widely used herbicide that is highly toxic to humans upon acute ingestion or chronic exposure. Here, the authors generate a photosensitive formulation that releases paraquat upon exposure to UV light or sunlight, which shows an improved safety profile in zebrafish and mouse models, while maintaining substantial herbicidal activity.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
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  • 2
    Publication Date: 2018-06-15
    Description: Objectives Although sleep, chronic disease and its related mortality are extensively studied areas, the association between stroke and sleep duration is relatively unknown. The aim of this study was to investigate the association between long and short sleep duration and stroke prevalence. Design A cross-sectional survey study. Setting and participants Adult surveyees (aged ≥19 years) who answered items relating to sleep duration and stroke in the 2010–2014 Korean National Health and Nutrition Surveys (n=17 601). Outcome measures Participants were divided into three groups by sleep duration (short: ≤6 hours/day, normal: 7–8 hours/day and long: ≥9 hours/day). Stroke prevalence in each sleep duration group was compared using logistic regression analysis, and sociodemographic characteristics, medical history, lifestyle habits and mental health factors were set as confounding variables. Results On adjusting for sex and age, each sleep-duration group displayed significantly different health-related characteristics. The short sleep and long sleep duration groups indicated significantly higher psychological factors for stress perception, depressive symptoms and psychiatric counselling compared with the normal sleep duration group. On adjustment of various confounders, the long sleep duration group demonstrated significantly higher ORs for stroke compared with the normal sleep duration group (OR 1.96, 95% CI 1.06 to 3.61). Also, when stratified by sex, men did not exhibit differences in stroke prevalence by sleep duration, but women showed higher stroke prevalence in the long sleep duration group compared with normal sleep duration (OR 2.94, 95% CI 1.21 to 7.17). Conclusions Longer sleep duration was associated with higher stroke prevalence, and this trend was more pronounced in women.
    Keywords: Open access, Epidemiology
    Electronic ISSN: 2044-6055
    Topics: Medicine
    Published by BMJ Publishing
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  • 3
    Publication Date: 2012-11-06
    Description: Models of unregulated nitric oxide (NO) diffusion do not consistently account for the biochemistry of NO synthase (NOS)-dependent signalling in many cell systems. For example, endothelial NOS controls blood pressure, blood flow and oxygen delivery through its effect on vascular smooth muscle tone, but the regulation of these processes is not adequately explained by simple NO diffusion from endothelium to smooth muscle. Here we report a new model for the regulation of NO signalling by demonstrating that haemoglobin (Hb) alpha (encoded by the HBA1 and HBA2 genes in humans) is expressed in human and mouse arterial endothelial cells and enriched at the myoendothelial junction, where it regulates the effects of NO on vascular reactivity. Notably, this function is unique to Hb alpha and is abrogated by its genetic depletion. Mechanistically, endothelial Hb alpha haem iron in the Fe(3+) state permits NO signalling, and this signalling is shut off when Hb alpha is reduced to the Fe(2+) state by endothelial cytochrome b5 reductase 3 (CYB5R3, also known as diaphorase 1). Genetic and pharmacological inhibition of CYB5R3 increases NO bioactivity in small arteries. These data reveal a new mechanism by which the regulation of the intracellular Hb alpha oxidation state controls NOS signalling in non-erythroid cells. This model may be relevant to haem-containing globins in a broad range of NOS-containing somatic cells.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3531883/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3531883/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Straub, Adam C -- Lohman, Alexander W -- Billaud, Marie -- Johnstone, Scott R -- Dwyer, Scott T -- Lee, Monica Y -- Bortz, Pamela Schoppee -- Best, Angela K -- Columbus, Linda -- Gaston, Benjamin -- Isakson, Brant E -- HL007284/HL/NHLBI NIH HHS/ -- HL059337/HL/NHLBI NIH HHS/ -- HL088554/HL/NHLBI NIH HHS/ -- HL101871/HL/NHLBI NIH HHS/ -- HL107963/HL/NHLBI NIH HHS/ -- HL112904/HL/NHLBI NIH HHS/ -- R00 HL112904/HL/NHLBI NIH HHS/ -- R01 HL088554/HL/NHLBI NIH HHS/ -- R21 HL107963/HL/NHLBI NIH HHS/ -- England -- Nature. 2012 Nov 15;491(7424):473-7. doi: 10.1038/nature11626. Epub 2012 Oct 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, Virginia 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23123858" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic alpha-1 Receptor Agonists/pharmacology ; Animals ; Cells, Cultured ; Diffusion ; Endothelial Cells/drug effects/enzymology/*metabolism ; Gene Expression Profiling ; *Gene Expression Regulation/drug effects ; Hemoglobins/genetics/*metabolism ; Humans ; Iron/chemistry ; Mice ; Nitric Oxide/*metabolism ; Nitric Oxide Synthase/metabolism ; Oxidation-Reduction ; Peptide Fragments/genetics/*metabolism ; Phenylephrine/pharmacology ; *Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
    Publication Date: 2015-08-13
    Description: Breast cancer is the most frequent cancer in women and consists of heterogeneous types of tumours that are classified into different histological and molecular subtypes. PIK3CA and P53 (also known as TP53) are the two most frequently mutated genes and are associated with different types of human breast cancers. The cellular origin and the mechanisms leading to PIK3CA-induced tumour heterogeneity remain unknown. Here we used a genetic approach in mice to define the cellular origin of Pik3ca-derived tumours and the impact of mutations in this gene on tumour heterogeneity. Surprisingly, oncogenic Pik3ca(H1047R) mutant expression at physiological levels in basal cells using keratin (K)5-CreER(T2) mice induced the formation of luminal oestrogen receptor (ER)-positive/progesterone receptor (PR)-positive tumours, while its expression in luminal cells using K8-CReER(T2) mice gave rise to luminal ER(+)PR(+) tumours or basal-like ER(-)PR(-) tumours. Concomitant deletion of p53 and expression of Pik3ca(H1047R) accelerated tumour development and induced more aggressive mammary tumours. Interestingly, expression of Pik3ca(H1047R) in unipotent basal cells gave rise to luminal-like cells, while its expression in unipotent luminal cells gave rise to basal-like cells before progressing into invasive tumours. Transcriptional profiling of cells that underwent cell fate transition upon Pik3ca(H1047R) expression in unipotent progenitors demonstrated a profound oncogene-induced reprogramming of these newly formed cells and identified gene signatures characteristic of the different cell fate switches that occur upon Pik3ca(H1047R) expression in basal and luminal cells, which correlated with the cell of origin, tumour type and different clinical outcomes. Altogether our study identifies the cellular origin of Pik3ca-induced tumours and reveals that oncogenic Pik3ca(H1047R) activates a multipotent genetic program in normally lineage-restricted populations at the early stage of tumour initiation, setting the stage for future intratumoural heterogeneity. These results have important implications for our understanding of the mechanisms controlling tumour heterogeneity and the development of new strategies to block PIK3CA breast cancer initiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Keymeulen, Alexandra -- Lee, May Yin -- Ousset, Marielle -- Brohee, Sylvain -- Rorive, Sandrine -- Giraddi, Rajshekhar R -- Wuidart, Aline -- Bouvencourt, Gaelle -- Dubois, Christine -- Salmon, Isabelle -- Sotiriou, Christos -- Phillips, Wayne A -- Blanpain, Cedric -- England -- Nature. 2015 Sep 3;525(7567):119-23. doi: 10.1038/nature14665. Epub 2015 Aug 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Universite Libre de Bruxelles, IRIBHM, Brussels B-1070, Belgium. ; Institut Jules Bordet, Universite Libre de Bruxelles, Brussels B-1000, Belgium. ; Department of Pathology, Erasme Hospital, Universite Libre de Bruxelles, Brussels B-1070, Belgium. ; DIAPATH - Center for Microscopy and Molecular Imaging (CMMI), Gosselies B-6041, Belgium. ; Surgical Oncology Research Laboratory, Peter MacCallum Cancer Centre, Melbourne 3002, Australia. ; Sir Peter MacCallum Department of Oncology, University of Melbourne, Parkville 3002, Australia. ; WELBIO, Universite Libre de Bruxelles, Brussels B-1070, Belgium.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26266985" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/*genetics/metabolism/*pathology ; Cell Differentiation/genetics ; Cell Division ; Cell Lineage ; Cell Transformation, Neoplastic ; Female ; Genes, p53/genetics ; Humans ; Mammary Neoplasms, Animal/*genetics/metabolism/*pathology ; Mice ; Mutation/genetics ; Neoplasm Invasiveness/genetics ; Phenotype ; Phosphatidylinositol 3-Kinases/*genetics/metabolism ; Receptors, Estrogen/metabolism ; Receptors, Progesterone/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2018-10-24
    Description: Aberrant activation of non-coding RNA targets of transcriptional elongation complexes contributes to TDP-43 toxicity Aberrant activation of non-coding RNA targets of transcriptional elongation complexes contributes to TDP-43 toxicity, Published online: 23 October 2018; doi:10.1038/s41467-018-06543-0 TDP-43 is associated with amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration with ubiquitinated inclusions (FTD-TDP). Here, the authors identify the transcriptional elongation factor Ell as a strong modifier of TDP-43-mediated neurodegeneration through the Ell transcriptional elongation complexes LEC and SEC.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
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  • 6
    Publication Date: 2018-10-12
    Description: Patient-derived frontotemporal lobar degeneration brain extracts induce formation and spreading of TDP-43 pathology in vivo Patient-derived frontotemporal lobar degeneration brain extracts induce formation and spreading of TDP-43 pathology in vivo, Published online: 11 October 2018; doi:10.1038/s41467-018-06548-9 Cell-to-cell transmission of TDP43 occurs in cell cultures and may contribute to pathological TDP43 propagation in FTLD-TDP. In this study, the authors demonstrate using mouse models that a single intracerebral injection of human brain-derived pathological TDP43 from FTLD-TDP cases initiates the process of seeding and spreading of TDP43 pathology in a spatio-temporal dependent manner in the brain.
    Electronic ISSN: 2041-1723
    Topics: Biology , Chemistry and Pharmacology , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2018-04-07
    Description: The Journal of Organic Chemistry DOI: 10.1021/acs.joc.8b00543
    Print ISSN: 0022-3263
    Electronic ISSN: 1520-6904
    Topics: Chemistry and Pharmacology
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  • 8
    Publication Date: 2018-03-13
    Description: Biomarkers for α-synuclein are needed for diagnosis and prognosis in Parkinson's disease (PD). Endogenous auto-antibodies to α-synuclein could serve as biomarkers for underlying synucleinopathy, but previous assessments of auto-antibodies have shown variability and inconsistent clinical correlations. We hypothesized that auto-antibodies to α-synuclein could be diagnostic for PD and explain its clinical heterogeneity. To test this hypothesis, we developed an enzyme-linked immunosorbent assay for measuring α-synuclein auto-antibodies in human samples. We evaluated 69 serum samples (16 healthy controls (HC) and 53 PD patients) and 145 CSF samples (52 HC and 93 PD patients) from our Institution. Both serum and CSF were available for 24 participants. Males had higher auto-antibody levels than females in both fluids. CSF auto-antibody levels were significantly higher in PD patients as compared to HC, whereas serum levels were not significantly different. CSF auto-antibody levels did not associate with amyloid-β 1-42 , total tau, or phosphorylated tau. CSF auto-antibody levels correlated with performance on the Montreal Cognitive Assessment, even when controlled for CSF amyloidβ 1-42 . CSF hemoglobin levels, as a proxy for contamination of CSF by blood during lumbar puncture, did not influence these observations. Using recombinant α-synuclein with N- and C-terminal truncations, we found that CSF auto-antibodies target amino acids 100 through 120 of α-synuclein. We conclude that endogenous CSF auto-antibodies are significantly higher in PD patients as compared to HC, suggesting that they could indicate the presence of underlying synucleinopathy. These auto-antibodies associate with poor cognition, independently of CSF amyloidβ 1-42 ., and target a select C-terminal region of α-synuclein. This article is protected by copyright. All rights reserved.
    Print ISSN: 0022-3042
    Electronic ISSN: 1471-4159
    Topics: Medicine
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  • 9
    Publication Date: 2018-02-21
    Description: Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy Microglia-mediated recovery from ALS-relevant motor neuron degeneration in a mouse model of TDP-43 proteinopathy, Published online: 20 February 2018; doi:10.1038/s41593-018-0083-7 Using an inducible mouse model of sporadic ALS, Spiller et al. show that spinal microgliosis is not a major feature of TDP-43-triggered disease. Instead, microglia mediate TDP-43 clearance and motor recovery, suggesting a neuroprotective role in ALS.
    Print ISSN: 1097-6256
    Electronic ISSN: 1546-1726
    Topics: Biology , Medicine
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  • 10
    ISSN: 1432-1106
    Keywords: Key words GABA ; Bromodeoxyuridine ; Proliferation ; Immunohistochemistry ; Retina ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The birthdates of GABAergic amacrine cells in the rat retina were investigated by immunocytochemistry using anti-GABA and anti-bromodeoxyuridine (BrdU) antisera. The ratio of co-localization of GABA to BrdU increased gradually from embryonic-day 13 (E13) and showed a peak value on E18 in the central retina and on E20 in the periphery. After birth, until postnatal-day 3 (P3), a few co-localized cells were observed in the inner nuclear layer (INL). However, in the peripheral retina, co-localized cells were observed in the INL and ganglion cell layer until P5. Our results suggest that the birthdates of GABA-immunoreactive cells vary, depending on cell-type and that there is a temporal lag in the GABA-immunoreactive cell production in the peripheral retina relative to the central retina.
    Type of Medium: Electronic Resource
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