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  • 1
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    Salinity effects on asexual reproduction of Carybdea sp. (Cnidaria: Cubozoa) (2014)
    Oxford University Press
    Details
    Publication Date: 2014-03-08
    Description: Medusa production in cubozoans may be associated with reduced-salinity waters. Asexual reproduction of Carybdea sp. differed at different salinities. The metamorphosis of Carybdea sp. polyps into medusae was accelerated at low salinity (32), while more polyps were budded from the original polyp at the highest salinity (38), probably due to prolonged metamorphosis. High-nutrient river discharge may provide favorable conditions for Carybdea sp. blooms.
    Print ISSN: 0142-7873
    Electronic ISSN: 1464-3774
    Topics: Biology
    Published by Oxford University Press
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  • 2
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    Chronic pro-oxidative state and mitochondrial dysfunctions are more pronounced in fibroblasts from Down syndrome foeti with congenital heart defects (2013)
    Oxford University Press
    Details
    Publication Date: 2013-02-22
    Description: Trisomy of chromosome 21 is associated to congenital heart defects in ~50% of affected newborns. Transcriptome analysis of hearts from trisomic human foeti demonstrated that genes involved in mitochondrial function are globally downregulated with respect to controls, suggesting an impairment of mitochondrial function. We investigated here the properties of mitochondria in fibroblasts from trisomic foeti with and without cardiac defects. Together with the upregulation of Hsa21 genes and the downregulation of nuclear encoded mitochondrial genes, an abnormal mitochondrial cristae morphology was observed in trisomic samples. Furthermore, impairment of mitochondrial respiratory activity, specific inhibition of complex I, enhanced reactive oxygen species production and increased levels of intra-mitochondrial calcium were demonstrated. Seemingly, mitochondrial dysfunction was more severe in fibroblasts from cardiopathic trisomic foeti that presented a more pronounced pro-oxidative state. The data suggest that an altered bioenergetic background in trisomy 21 foeti might be among the factors responsible for a more severe phenotype. Since the mitochondrial functional alterations might be rescued following pharmacological treatments, these results are of interest in the light of potential therapeutic interventions.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 3
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    Genes, Vol. 10, Pages 93: H3K9 Promotes Under-Replication of Pericentromeric Heterochromatin in Drosophila Salivary Gland Polytene Chromosomes (2019)
    MDPI
    In: Genes
    Details
    Publication Date: 2019
    Description: Chromatin structure and its organization contributes to the proper regulation and timing of DNA replication. Yet, the precise mechanism by which chromatin contributes to DNA replication remains incompletely understood. This is particularly true for cell types that rely on polyploidization as a developmental strategy for growth and high biosynthetic capacity. During Drosophila larval development, cells of the salivary gland undergo endoreplication, repetitive rounds of DNA synthesis without intervening cell division, resulting in ploidy values of ~1350C. S phase of these endocycles displays a reproducible pattern of early and late replicating regions of the genome resulting from the activity of the same replication initiation factors that are used in diploid cells. However, unlike diploid cells, the latest replicating regions of polyploid salivary gland genomes, composed primarily of pericentric heterochromatic enriched in H3K9 methylation, are not replicated each endocycle, resulting in under-replicated domains with reduced ploidy. Here, we employ a histone gene replacement strategy in Drosophila to demonstrate that mutation of a histone residue important for heterochromatin organization and function (H3K9) but not mutation of a histone residue important for euchromatin function (H4K16), disrupts proper endoreplication in Drosophila salivary gland polyploid genomes thereby leading to DNA copy gain in pericentric heterochromatin. These findings reveal that H3K9 is necessary for normal levels of under-replication of pericentric heterochromatin and suggest that under-replication at pericentric heterochromatin is mediated through H3K9 methylation.
    Electronic ISSN: 2073-4425
    Topics: Biology
    Published by MDPI
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  • 4
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    Keeping the U.S. a world leader in science (2007)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2007-07-14
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gentile, James M -- New York, N.Y. -- Science. 2007 Jul 13;317(5835):194.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17626863" target="_blank"〉PubMed〈/a〉
    Keywords: Financing, Government ; Foundations ; Fund Raising ; *Research Support as Topic ; *Science ; United States
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    MED12, the mediator complex subunit 12 gene, is mutated at high frequency in uterine leiomyomas (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-08-27
    Description: Uterine leiomyomas, or fibroids, are benign tumors that affect millions of women worldwide and that can cause considerable morbidity. To study the genetic basis of this tumor type, we examined 18 uterine leiomyomas derived from 17 different patients by exome sequencing and identified tumor-specific mutations in the mediator complex subunit 12 (MED12) gene in 10. Through analysis of 207 additional tumors, we determined that MED12 is altered in 70% (159 of 225) of tumors from a total of 80 patients. The Mediator complex is a 26-subunit transcriptional regulator that bridges DNA regulatory sequences to the RNA polymerase II initiation complex. All mutations resided in exon 2, suggesting that aberrant function of this region of MED12 contributes to tumorigenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makinen, Netta -- Mehine, Miika -- Tolvanen, Jaana -- Kaasinen, Eevi -- Li, Yilong -- Lehtonen, Heli J -- Gentile, Massimiliano -- Yan, Jian -- Enge, Martin -- Taipale, Minna -- Aavikko, Mervi -- Katainen, Riku -- Virolainen, Elina -- Bohling, Tom -- Koski, Taru A -- Launonen, Virpi -- Sjoberg, Jari -- Taipale, Jussi -- Vahteristo, Pia -- Aaltonen, Lauri A -- New York, N.Y. -- Science. 2011 Oct 14;334(6053):252-5. doi: 10.1126/science.1208930. Epub 2011 Aug 25.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medical Genetics, Genome-Scale Biology Research Program, University of Helsinki, Helsinki, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21868628" target="_blank"〉PubMed〈/a〉
    Keywords: Codon ; Exons ; Female ; Gene Expression Profiling ; Humans ; INDEL Mutation ; Introns ; Leiomyoma/*genetics/metabolism ; Mediator Complex/*genetics ; Mutation ; Mutation, Missense ; Signal Transduction ; Uterine Neoplasms/*genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Education. Teaching in a research context (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-12-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wood, William B -- Gentile, James M -- New York, N.Y. -- Science. 2003 Nov 28;302(5650):1510.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular, Cellular and Developmental Biology, University of Colorado, Boulder, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14645829" target="_blank"〉PubMed〈/a〉
    Keywords: Academies and Institutes ; Biological Science Disciplines/*education ; *Biomedical Research ; Curriculum ; *Faculty ; National Academy of Sciences (U.S.) ; Physics/education ; Research Personnel ; Teaching/*methods ; Teaching Materials ; United States ; Universities
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    Mucus enhances gut homeostasis and oral tolerance by delivering immunoregulatory signals (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-09-28
    Description: A dense mucus layer in the large intestine prevents inflammation by shielding the underlying epithelium from luminal bacteria and food antigens. This mucus barrier is organized around the hyperglycosylated mucin MUC2. Here we show that the small intestine has a porous mucus layer, which permitted the uptake of MUC2 by antigen-sampling dendritic cells (DCs). Glycans associated with MUC2 imprinted DCs with anti-inflammatory properties by assembling a galectin-3-Dectin-1-FcgammaRIIB receptor complex that activated beta-catenin. This transcription factor interfered with DC expression of inflammatory but not tolerogenic cytokines by inhibiting gene transcription through nuclear factor kappaB. MUC2 induced additional conditioning signals in intestinal epithelial cells. Thus, mucus does not merely form a nonspecific physical barrier, but also constrains the immunogenicity of gut antigens by delivering tolerogenic signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005805/" 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/PMC4005805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shan, Meimei -- Gentile, Maurizio -- Yeiser, John R -- Walland, A Cooper -- Bornstein, Victor U -- Chen, Kang -- He, Bing -- Cassis, Linda -- Bigas, Anna -- Cols, Montserrat -- Comerma, Laura -- Huang, Bihui -- Blander, J Magarian -- Xiong, Huabao -- Mayer, Lloyd -- Berin, Cecilia -- Augenlicht, Leonard H -- Velcich, Anna -- Cerutti, Andrea -- AI073899/AI/NIAID NIH HHS/ -- AI095245/AI/NIAID NIH HHS/ -- AI57653/AI/NIAID NIH HHS/ -- AI61093/AI/NIAID NIH HHS/ -- AI74378/AI/NIAID NIH HHS/ -- AI95613/AI/NIAID NIH HHS/ -- AI96187/AI/NIAID NIH HHS/ -- DK072201/DK/NIDDK NIH HHS/ -- P01 AI061093/AI/NIAID NIH HHS/ -- P01 DK072201/DK/NIDDK NIH HHS/ -- P60 DK020541/DK/NIDDK NIH HHS/ -- R01 AI057653/AI/NIAID NIH HHS/ -- R01 AI093577/AI/NIAID NIH HHS/ -- U01 AI095613/AI/NIAID NIH HHS/ -- U19 AI096187/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):447-53. doi: 10.1126/science.1237910. Epub 2013 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendritic Cells/immunology ; Galectin 3/genetics/metabolism ; Glycosylation ; *Homeostasis ; Humans ; Immune Tolerance/genetics/*immunology ; Inflammation/immunology ; Intestinal Mucosa/immunology ; Intestine, Small/*immunology ; Lectins, C-Type/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mouth/*immunology ; Mucin-2/genetics/physiology ; Mucus/*immunology ; NF-kappa B/metabolism ; Receptors, IgG/genetics/metabolism ; Transcription, Genetic ; beta Catenin/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 8
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    Activation of 2-aminofluorene by cultured plant cells (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-03-25
    Description: Cultured tobacco plant cells activated 2-aminofluorene to an agent mutagenic to Salmonella typhimurium strain TA98. The plant activation of 2-aminofluorene is heat-inactivated and may not involve solely cytochrome P-450. The kinetics of activation demonstrated both time- and concentration-dependent responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plewa, M J -- Weaver, D L -- Blair, L C -- Gentile, J M -- ES02384/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1427-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6338591" target="_blank"〉PubMed〈/a〉
    Keywords: Biotransformation ; Cells, Cultured ; Fluorenes/*metabolism/pharmacology ; Kinetics ; Mutagenicity Tests ; Mutagens/*metabolism ; *Mutation ; *Plants, Toxic ; Salmonella typhimurium/drug effects ; Tobacco/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 9
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    Rfx6 directs islet formation and insulin production in mice and humans (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-02-12
    Description: Insulin from the beta-cells of the pancreatic islets of Langerhans controls energy homeostasis in vertebrates, and its deficiency causes diabetes mellitus. During embryonic development, the transcription factor neurogenin 3 (Neurog3) initiates the differentiation of the beta-cells and other islet cell types from pancreatic endoderm, but the genetic program that subsequently completes this differentiation remains incompletely understood. Here we show that the transcription factor Rfx6 directs islet cell differentiation downstream of Neurog3. Mice lacking Rfx6 failed to generate any of the normal islet cell types except for pancreatic-polypeptide-producing cells. In human infants with a similar autosomal recessive syndrome of neonatal diabetes, genetic mapping and subsequent sequencing identified mutations in the human RFX6 gene. These studies demonstrate a unique position for Rfx6 in the hierarchy of factors that coordinate pancreatic islet development in both mice and humans. Rfx6 could prove useful in efforts to generate beta-cells for patients with diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2896718/" 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/PMC2896718/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Smith, Stuart B -- Qu, Hui-Qi -- Taleb, Nadine -- Kishimoto, Nina Y -- Scheel, David W -- Lu, Yang -- Patch, Ann-Marie -- Grabs, Rosemary -- Wang, Juehu -- Lynn, Francis C -- Miyatsuka, Takeshi -- Mitchell, John -- Seerke, Rina -- Desir, Julie -- Vanden Eijnden, Serge -- Abramowicz, Marc -- Kacet, Nadine -- Weill, Jacques -- Renard, Marie-Eve -- Gentile, Mattia -- Hansen, Inger -- Dewar, Ken -- Hattersley, Andrew T -- Wang, Rennian -- Wilson, Maria E -- Johnson, Jeffrey D -- Polychronakos, Constantin -- German, Michael S -- P30 DK063720/DK/NIDDK NIH HHS/ -- P30 DK063720-045954/DK/NIDDK NIH HHS/ -- P30 DK063720-045955/DK/NIDDK NIH HHS/ -- P30 DK063720-045956/DK/NIDDK NIH HHS/ -- P30 DK063720-045957/DK/NIDDK NIH HHS/ -- P30 DK063720-045958/DK/NIDDK NIH HHS/ -- P30 DK063720-05/DK/NIDDK NIH HHS/ -- R01 DK021344/DK/NIDDK NIH HHS/ -- R01 DK021344-26/DK/NIDDK NIH HHS/ -- U19 DK061245/DK/NIDDK NIH HHS/ -- U19 DK061245-04/DK/NIDDK NIH HHS/ -- U19 DK061245-049001/DK/NIDDK NIH HHS/ -- Canadian Institutes of Health Research/Canada -- England -- Nature. 2010 Feb 11;463(7282):775-80. doi: 10.1038/nature08748.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Diabetes Center, University of California San Francisco, San Francisco, California 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20148032" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basic Helix-Loop-Helix Transcription Factors/deficiency/genetics/metabolism ; *Cell Differentiation ; DNA Mutational Analysis ; DNA-Binding Proteins/deficiency/genetics/*metabolism ; Diabetes Mellitus/congenital/genetics/metabolism/pathology ; Embryo, Mammalian/metabolism ; Female ; Fetus/metabolism ; Gene Expression Profiling ; Gene Expression Regulation, Developmental ; Genes, Recessive/genetics ; Genetic Testing ; Humans ; Infant, Newborn ; Insulin/*biosynthesis ; Islets of Langerhans/*cytology/embryology/*metabolism ; Male ; Mice ; NIH 3T3 Cells ; Nerve Tissue Proteins/deficiency/genetics/metabolism ; Organ Specificity ; Syndrome ; Transcription Factors/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 10
    Electronic Resource
    Electronic Resource
    Pharmacokinetics of teicoplanin in patients on continuous ambulatory peritoneal dialysis (1986)
    Springer
    European journal of clinical pharmacology 31 (1986), S. 501-504 
    Details
    ISSN: 1432-1041
    Keywords: teicoplanin ; continuous ambulatory peritoneal dialysis ; pharmacokinetics ; antibiotic
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary We have studied the pharmacokinetics of teicoplanin, a new glycopeptide antibiotic active against Gram-positive aerobic and anaerobic bacteria, in five patients with end-stage renal disease on continuous ambulatory peritoneal dialysis (CAPD). Although teicoplanin was eliminated in the peritoneal fluid, relatively little was recovered (6.8±1.2% of the given dose). The following values were obtained: elimination half-time 102–347 h; total body clearance 4.16–7.38 ml·h−1·kg−1, peritoneal clearance 0.31–0.37 ml·h−1·kg−1. Because the elimination of teicoplanin is about four times less in patients undergoing CAPD compared with subjects with normal renal function, the dose of teicoplanin should be reduced appropriately in such cases.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00613532
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