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  • 1
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    miR-155 nanoparticle therapy in lymphoma [Applied Biological Sciences] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-06-27
    Description: MicroRNA-155 (miR-155) is an oncogenic microRNA that regulates several pathways involved in cell division and immunoregulation. It is overexpressed in numerous cancers, is often correlated with poor prognosis, and is thus a key target for future therapies. In this work we show that overexpression of miR-155 in lymphoid tissues results in disseminated lymphoma characterized by a clonal, transplantable pre-B-cell population of neoplastic lymphocytes. Withdrawal of miR-155 in mice with established disease results in rapid regression of lymphadenopathy, in part because of apoptosis of the malignant lymphocytes, demonstrating that these tumors are dependent on miR-155 expression. We show that systemic delivery of antisense peptide nucleic acids encapsulated in unique polymer nanoparticles inhibits miR-155 and slows the growth of these “addicted” pre-B-cell tumors in vivo, suggesting a promising therapeutic option for lymphoma/leukemia.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 2
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    Caspases 3 and 7: key mediators of mitochondrial events of apoptosis (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-02-14
    Description: The current model of apoptosis holds that upstream signals lead to activation of downstream effector caspases. We generated mice deficient in the two effectors, caspase 3 and caspase 7, which died immediately after birth with defects in cardiac development. Fibroblasts lacking both enzymes were highly resistant to both mitochondrial and death receptor-mediated apoptosis, displayed preservation of mitochondrial membrane potential, and had defective nuclear translocation of apoptosis-inducing factor (AIF). Furthermore, the early apoptotic events of Bax translocation and cytochrome c release were also delayed. We conclude that caspases 3 and 7 are critical mediators of mitochondrial events of apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3738210/" 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/PMC3738210/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lakhani, Saquib A -- Masud, Ali -- Kuida, Keisuke -- Porter, George A Jr -- Booth, Carmen J -- Mehal, Wajahat Z -- Inayat, Irteza -- Flavell, Richard A -- 1 K08 HD044580/HD/NICHD NIH HHS/ -- 5 K12 HD01401/HD/NICHD NIH HHS/ -- K08 DK002965/DK/NIDDK NIH HHS/ -- K08 DK002965-04/DK/NIDDK NIH HHS/ -- K12 HD00850/HD/NICHD NIH HHS/ -- NIDDK P30-34989/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 2006 Feb 10;311(5762):847-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16469926" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Inducing Factor/metabolism ; Caspase 3 ; Caspase 7 ; Caspases/deficiency/*metabolism ; Cell Nucleus/metabolism ; Cell Shape ; Cell Survival ; Cells, Cultured ; Cytochromes c/metabolism ; DNA Fragmentation ; Female ; Fibroblasts/cytology ; Heart/embryology ; Heart Defects, Congenital/etiology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria/metabolism/*physiology ; Mitochondrial Membranes/physiology ; Permeability ; T-Lymphocytes/cytology ; bcl-2-Associated X Protein/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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  • 3
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    IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-10-19
    Description: Chronic mucosal inflammation and tissue damage predisposes patients to the development of colorectal cancer. This association could be explained by the hypothesis that the same factors and pathways important for wound healing also promote tumorigenesis. A sensor of tissue damage should induce these factors to promote tissue repair and regulate their action to prevent development of cancer. Interleukin 22 (IL-22), a cytokine of the IL-10 superfamily, has an important role in colonic epithelial cell repair, and its levels are increased in the blood and intestine of inflammatory bowel disease patients. This cytokine can be neutralized by the soluble IL-22 receptor, known as the IL-22 binding protein (IL-22BP, also known as IL22RA2); however, the significance of endogenous IL-22BP in vivo and the pathways that regulate this receptor are unknown. Here we describe that IL-22BP has a crucial role in controlling tumorigenesis and epithelial cell proliferation in the colon. IL-22BP is highly expressed by dendritic cells in the colon in steady-state conditions. Sensing of intestinal tissue damage via the NLRP3 or NLRP6 inflammasomes led to an IL-18-dependent downregulation of IL-22BP, thereby increasing the ratio of IL-22/IL-22BP. IL-22, which is induced during intestinal tissue damage, exerted protective properties during the peak of damage, but promoted tumour development if uncontrolled during the recovery phase. Thus, the IL-22-IL-22BP axis critically regulates intestinal tissue repair and tumorigenesis in the colon.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493690/" 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/PMC3493690/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huber, Samuel -- Gagliani, Nicola -- Zenewicz, Lauren A -- Huber, Francis J -- Bosurgi, Lidia -- Hu, Bo -- Hedl, Matija -- Zhang, Wei -- O'Connor, William Jr -- Murphy, Andrew J -- Valenzuela, David M -- Yancopoulos, George D -- Booth, Carmen J -- Cho, Judy H -- Ouyang, Wenjun -- Abraham, Clara -- Flavell, Richard A -- DK-P30-34989/DK/NIDDK NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- R01 DK077905/DK/NIDDK NIH HHS/ -- R01DK077905/DK/NIDDK NIH HHS/ -- U19 AI082713/AI/NIAID NIH HHS/ -- U19-AI082713/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Nov 8;491(7423):259-63. doi: 10.1038/nature11535. Epub 2012 Oct 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunobiology, Yale University School of Medicine, New Haven, Connecticut 06520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23075849" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Transformation, Neoplastic ; Colitis/complications/metabolism/pathology ; Colon/metabolism/pathology ; Colonic Neoplasms/complications/metabolism/pathology ; Disease Models, Animal ; Down-Regulation ; Epithelial Cells/metabolism/pathology ; Genes, APC ; Inflammasomes/*metabolism ; Interleukin-18/metabolism ; Interleukins/deficiency/genetics/metabolism ; Intestines/*metabolism/*pathology ; Mice ; Mice, Knockout ; Receptors, Interleukin/deficiency/genetics/*metabolism ; Time Factors ; Weight Loss
    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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  • 4
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    GBP5 promotes NLRP3 inflammasome assembly and immunity in mammals (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-03-31
    Description: Inflammasomes are sensory complexes that alert the immune system to the presence of infection or tissue damage. These complexes assemble NLR (nucleotide binding and oligomerization, leucine-rich repeat) or ALR (absent in melanoma 2-like receptor) proteins to activate caspase-1 cleavage and interleukin (IL)-1beta/IL-18 secretion. Here, we identified a non-NLR/ALR human protein that stimulates inflammasome assembly: guanylate binding protein 5 (GBP5). GBP5 promoted selective NLRP3 inflammasome responses to pathogenic bacteria and soluble but not crystalline inflammasome priming agents. Generation of Gbp5(-/-) mice revealed pronounced caspase-1 and IL-1beta/IL-18 cleavage defects in vitro and impaired host defense and Nlrp3-dependent inflammatory responses in vivo. Thus, GBP5 serves as a unique rheostat for NLRP3 inflammasome activation and extends our understanding of the inflammasome complex beyond its core machinery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shenoy, Avinash R -- Wellington, David A -- Kumar, Pradeep -- Kassa, Hilina -- Booth, Carmen J -- Cresswell, Peter -- MacMicking, John D -- R01 AI068041-06/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Apr 27;336(6080):481-5. doi: 10.1126/science.1217141. Epub 2012 Mar 29.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22461501" target="_blank"〉PubMed〈/a〉
    Keywords: Alum Compounds ; Animals ; Apoptosis Regulatory Proteins ; Carrier Proteins/genetics/*metabolism ; Caspase 1/metabolism ; Cell Line ; Cytoskeletal Proteins/metabolism ; GTP-Binding Proteins/chemistry/genetics/*metabolism ; Humans ; Inflammasomes/*metabolism ; Interferon-gamma/immunology ; Interleukin-1beta/secretion ; Lipopolysaccharides/immunology ; Listeria monocytogenes ; Listeriosis/immunology ; Macrophages/immunology/*metabolism ; Mice ; Protein Multimerization ; RNA Interference ; Salmonella typhimurium/immunology ; Uric Acid
    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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    Gut microbiota. Antimicrobial peptide resistance mediates resilience of prominent gut commensals during inflammation (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-01-13
    Description: Resilience to host inflammation and other perturbations is a fundamental property of gut microbial communities, yet the underlying mechanisms are not well understood. We have found that human gut microbes from all dominant phyla are resistant to high levels of inflammation-associated antimicrobial peptides (AMPs) and have identified a mechanism for lipopolysaccharide (LPS) modification in the phylum Bacteroidetes that increases AMP resistance by four orders of magnitude. Bacteroides thetaiotaomicron mutants that fail to remove a single phosphate group from their LPS were displaced from the microbiota during inflammation triggered by pathogen infection. These findings establish a mechanism that determines the stability of prominent members of a healthy microbiota during perturbation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4388331/" 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/PMC4388331/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cullen, T W -- Schofield, W B -- Barry, N A -- Putnam, E E -- Rundell, E A -- Trent, M S -- Degnan, P H -- Booth, C J -- Yu, H -- Goodman, A L -- AI064184/AI/NIAID NIH HHS/ -- AI76322/AI/NIAID NIH HHS/ -- DK089121/DK/NIDDK NIH HHS/ -- DP2 GM105456/GM/NIGMS NIH HHS/ -- GM103574/GM/NIGMS NIH HHS/ -- GM105456/GM/NIGMS NIH HHS/ -- R01 GM103574/GM/NIGMS NIH HHS/ -- T32 AI007640/AI/NIAID NIH HHS/ -- UL1 TR000142/TR/NCATS NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 9;347(6218):170-5. doi: 10.1126/science.1260580.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Molecular Biosciences and Institute of Cell and Molecular Biology, University of Texas, Austin, TX 78712, USA. ; Department of Microbiology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA. ; Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06520, USA. ; Cancer Epidemiology Program, University of Hawaii Cancer Center, Honolulu, HI 96813, USA. ; Department of Microbial Pathogenesis, Yale University School of Medicine, New Haven, CT 06520, USA. Microbial Sciences Institute, Yale University School of Medicine, New Haven, CT 06520, USA. andrew.goodman@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25574022" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antimicrobial Cationic Peptides ; Bacteroides/*drug effects/genetics/physiology ; Colitis/*microbiology ; Drug Resistance, Bacterial/*genetics ; Escherichia coli/drug effects/physiology ; Gastrointestinal Tract/*microbiology ; Germ-Free Life ; Humans ; Lipid A/metabolism ; Mice ; Microbiota/*drug effects/genetics/physiology ; Phosphoric Monoester Hydrolases/genetics/*physiology ; Polymyxin B/*pharmacology ; Symbiosis
    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
    Electronic Resource
    Electronic Resource
    Positive and negative impacts of longwall mine subsidence on a sandstone aquifer (1998)
    Springer
    Environmental geology 34 (1998), S. 223-233 
    Details
    ISSN: 1432-0495
    Keywords: Key words Aquifer properties ; Mining ; Subsidence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences
    Notes: Abstract  Subsidence due to longwall underground coal mining changes the hydraulic properties, heads, yields, and in some cases the groundwater chemistry of overlying bedrock aquifers. A 7-year study of a sandstone aquifer overlying an active longwall mine in Illinois has supported a comprehensive model of these impacts. Subsidence caused increases in permeability and storativity over the longwall panel. These changes initially caused a major decline in water levels in the sandstone, but the aquifer recovered slightly within a few months and fully within several years after mining. The enhanced hydraulic properties combined with potentiometric recovery resulted in a zone of greater well yield. However, at sites with very poor transmissivity and inadequate recharge pathways, recovery may not occur. Also, at the study site, the physical enhancement was accompanied by a deterioration in groundwater quality from slightly brackish, sodium bicarbonate water to more brackish water with increased sulfate levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002540050274
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  • 7
    Electronic Resource
    Electronic Resource
    Groundwater geochemistry in shallow aquifers above longwall mines in Illinois, USA (1999)
    Springer
    Hydrogeology journal 7 (1999), S. 561-575 
    Details
    ISSN: 1435-0157
    Keywords: Key words coalfield hydrogeology ; subsidence ; mining ; hydrochemistry ; USA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Geosciences
    Description / Table of Contents: Résumé Les aquifères situés au-dessus de mines de charbon et soumis à de forts pompages ne sont pas affectés par le drainage minier, mais peuvent montrer des modifications du chimisme des eaux souterraines dues à celles de l'écoulement souterrain provoquées par l'abaissement piézométrique au niveau de la mine. Dans deux sites miniers en activité de l'Illinois (États-Unis), des aquifères de moraines glaciaires n'ont pas, de façon générale, été affectés par l'exploitation minière; mais la géochimie des aquifères du substratum s'est modifiée lors de la remontée de la nappe, après arrêt de l'exploitation. Sur le site de Jefferson, où l'exploitation était pratiquée sur un large front, des eaux saumâtres, fortement sulfatées, existant dans les marnes du sommet du substratum, ont présenté très brièvement de plus faibles minéralisations après l'arrêt de la mine, du fait de l'accroissement de la recharge à partir de l'aquifère sus-jacent, tandis que la minéralisation et les sulfates ont augmenté dans les eaux bicarbonatées sodiques des grès sous-jacents, à cause de la drainance des marnes et de venues latérales d'eaux dans les grès. Sur le site de Saline, les grès contenaient des eaux de minéralisation variant de saumâtre à faciès chloruré sodique à douce à faciès bicarbonaté sodique. La remontée de la nappe après l'arrêt de l'exploitation a été minimale et les eaux ont subi des changements de qualité mineurs. L'exploitation minière sur un large front de taille affecte le chimisme des eaux à cause de la fracturation liée à l'effondrement, qui favorise l'augmentation de la drainance à l'aval à partir des formations sus-jacentes, et à cause de la dépression piézométrique temporaire et de la remontée consécutive, lorsque les eaux des zones voisines de l'aquifère rechargent la zone affectée au-dessus et à côté de la mine.
    Notes: Abstract  Aquifers above high-extraction underground coal mines are not affected by mine drainage, but they may still exhibit changes in groundwater chemistry due to alterations in groundwater flow induced by mine subsidence. At two active longwall mine sites in Illinois, USA, glacial-drift aquifers were largely unaffected by mining, but the geochemistry of the bedrock aquifers changed during the post-mining water-level recovery. At the Jefferson site, brackish, high-sulfate water present in the upper bedrock shale briefly had lower values of total dissolved solids (TDS) after mining due to increased recharge from the overlying drift, whereas TDS and sulfate increased in the sodium-bicarbonate water present in the underlying sandstone due to downward leakage from the shale and lateral inflow of water through the sandstone. At the Saline site, sandstones contained water ranging from brackish sodium-chloride to fresh sodium-bicarbonate type. Post-mining recovery of the potentiometric levels was minimal, and the water had minor quality changes. Longwall mining affects geochemistry due to subsidence-related fracturing, which increases downward leakage from overlying units, and due to the temporary potentiometric depression and subsequent recovery, whereby water from surrounding areas of the aquifer recharges the affected zone above and adjacent to the mine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100400050229
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  • 8
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    Inflammation-induced tumorigenesis in the colon is regulated by caspase-1 and NLRC4 (2010)
    National Academy of Sciences
    Details
    Publication Date: 2010-11-30
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    Nanoparticle-based therapy in an in vivo microRNA-155 (miR-155)-dependent mouse model of lymphoma (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-06-08
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Attenuation of signaling pathways stimulated by pathologically activated FGF-receptor 2 mutants prevents craniosynostosis (2006)
    National Academy of Sciences
    Details
    Publication Date: 2006-11-28
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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