ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Humans  (8)
  • 550 - Earth sciences  (7)
  • Aerospace Medicine
  • Age determination
  • Biological data
  • 2010-2014  (17)
  • 1
    facet.materialart.
    Unknown
    S-glutathionylation uncouples eNOS and regulates its cellular and vascular function (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-12-24
    Description: Endothelial nitric oxide synthase (eNOS) is critical in the regulation of vascular function, and can generate both nitric oxide (NO) and superoxide (O(2)(*-)), which are key mediators of cellular signalling. In the presence of Ca(2+)/calmodulin, eNOS produces NO, endothelial-derived relaxing factor, from l-arginine (l-Arg) by means of electron transfer from NADPH through a flavin containing reductase domain to oxygen bound at the haem of an oxygenase domain, which also contains binding sites for tetrahydrobiopterin (BH(4)) and l-Arg. In the absence of BH(4), NO synthesis is abrogated and instead O(2)(*-) is generated. While NOS dysfunction occurs in diseases with redox stress, BH(4) repletion only partly restores NOS activity and NOS-dependent vasodilation. This suggests that there is an as yet unidentified redox-regulated mechanism controlling NOS function. Protein thiols can undergo S-glutathionylation, a reversible protein modification involved in cellular signalling and adaptation. Under oxidative stress, S-glutathionylation occurs through thiol-disulphide exchange with oxidized glutathione or reaction of oxidant-induced protein thiyl radicals with reduced glutathione. Cysteine residues are critical for the maintenance of eNOS function; we therefore speculated that oxidative stress could alter eNOS activity through S-glutathionylation. Here we show that S-glutathionylation of eNOS reversibly decreases NOS activity with an increase in O(2)(*-) generation primarily from the reductase, in which two highly conserved cysteine residues are identified as sites of S-glutathionylation and found to be critical for redox-regulation of eNOS function. We show that eNOS S-glutathionylation in endothelial cells, with loss of NO and gain of O(2)(*-) generation, is associated with impaired endothelium-dependent vasodilation. In hypertensive vessels, eNOS S-glutathionylation is increased with impaired endothelium-dependent vasodilation that is restored by thiol-specific reducing agents, which reverse this S-glutathionylation. Thus, S-glutathionylation of eNOS is a pivotal switch providing redox regulation of cellular signalling, endothelial function and vascular tone.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370391/" 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/PMC3370391/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Chun-An -- Wang, Tse-Yao -- Varadharaj, Saradhadevi -- Reyes, Levy A -- Hemann, Craig -- Talukder, M A Hassan -- Chen, Yeong-Renn -- Druhan, Lawrence J -- Zweier, Jay L -- K99 HL103846/HL/NHLBI NIH HHS/ -- K99 HL103846-02/HL/NHLBI NIH HHS/ -- R01 HL038324/HL/NHLBI NIH HHS/ -- R01 HL038324-20/HL/NHLBI NIH HHS/ -- R01 HL063744/HL/NHLBI NIH HHS/ -- R01 HL063744-09/HL/NHLBI NIH HHS/ -- R01HL103846/HL/NHLBI NIH HHS/ -- R01HL38324/HL/NHLBI NIH HHS/ -- R01HL63744/HL/NHLBI NIH HHS/ -- R01HL65608/HL/NHLBI NIH HHS/ -- R01HL83237/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Dec 23;468(7327):1115-8. doi: 10.1038/nature09599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Davis Heart and Lung Research Institute and Division of Cardiovascular Medicine, Department of Internal Medicine, College of Medicine, Ohio State University, Columbus, Ohio 43210, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21179168" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; Cells, Cultured ; Dithiothreitol/pharmacology ; Endothelial Cells/metabolism ; Endothelium, Vascular/*metabolism ; Glutathione/*metabolism ; Humans ; Male ; Mercaptoethanol/pharmacology ; Mutation ; Nitric Oxide Synthase Type III/genetics/*metabolism ; Oxidation-Reduction ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Rats, Sprague-Dawley ; Reducing Agents/pharmacology ; Signal Transduction ; Vasodilation/physiology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 2
    facet.materialart.
    Unknown
    The shared antibiotic resistome of soil bacteria and human pathogens (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-01
    Description: Soil microbiota represent one of the ancient evolutionary origins of antibiotic resistance and have been proposed as a reservoir of resistance genes available for exchange with clinical pathogens. Using a high-throughput functional metagenomic approach in conjunction with a pipeline for the de novo assembly of short-read sequence data from functional selections (termed PARFuMS), we provide evidence for recent exchange of antibiotic resistance genes between environmental bacteria and clinical pathogens. We describe multidrug-resistant soil bacteria containing resistance cassettes against five classes of antibiotics (beta-lactams, aminoglycosides, amphenicols, sulfonamides, and tetracyclines) that have perfect nucleotide identity to genes from diverse human pathogens. This identity encompasses noncoding regions as well as multiple mobilization sequences, offering not only evidence of lateral exchange but also a mechanism by which antibiotic resistance disseminates.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4070369/" 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/PMC4070369/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Forsberg, Kevin J -- Reyes, Alejandro -- Wang, Bin -- Selleck, Elizabeth M -- Sommer, Morten O A -- Dantas, Gautam -- T32 GM007067/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1107-11. doi: 10.1126/science.1220761.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St. Louis, MO 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22936781" target="_blank"〉PubMed〈/a〉
    Keywords: Aminoglycosides/pharmacology ; Anti-Bacterial Agents/*pharmacology ; Bacteria/*drug effects/*genetics/pathogenicity ; Base Sequence ; Drug Resistance, Multiple, Bacterial/*genetics ; High-Throughput Screening Assays ; Humans ; Metagenome/*drug effects/*genetics ; Metagenomics ; Molecular Sequence Data ; *Soil Microbiology ; Sulfonamides/pharmacology ; Tetracyclines/pharmacology ; beta-Lactams/pharmacology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 3
    facet.materialart.
    Unknown
    Viruses in the faecal microbiota of monozygotic twins and their mothers (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-07-16
    Description: Viral diversity and life cycles are poorly understood in the human gut and other body habitats. Phages and their encoded functions may provide informative signatures of a human microbiota and of microbial community responses to various disturbances, and may indicate whether community health or dysfunction is manifest after apparent recovery from a disease or therapeutic intervention. Here we report sequencing of the viromes (metagenomes) of virus-like particles isolated from faecal samples collected from healthy adult female monozygotic twins and their mothers at three time points over a one-year period. We compared these data sets with data sets of sequenced bacterial 16S ribosomal RNA genes and total-faecal-community DNA. Co-twins and their mothers share a significantly greater degree of similarity in their faecal bacterial communities than do unrelated individuals. In contrast, viromes are unique to individuals regardless of their degree of genetic relatedness. Despite remarkable interpersonal variations in viromes and their encoded functions, intrapersonal diversity is very low, with 〉95% of virotypes retained over the period surveyed, and with viromes dominated by a few temperate phages that exhibit remarkable genetic stability. These results indicate that a predatory viral-microbial dynamic, manifest in a number of other characterized environmental ecosystems, is notably absent in the very distal intestine.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2919852/" 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/PMC2919852/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reyes, Alejandro -- Haynes, Matthew -- Hanson, Nicole -- Angly, Florent E -- Heath, Andrew C -- Rohwer, Forest -- Gordon, Jeffrey I -- DK78669/DK/NIDDK NIH HHS/ -- P01 DK078669/DK/NIDDK NIH HHS/ -- P01 DK078669-03S1/DK/NIDDK NIH HHS/ -- England -- Nature. 2010 Jul 15;466(7304):334-8. doi: 10.1038/nature09199.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Genome Sciences and Systems Biology, Washington University School of Medicine, St Louis, Missouri 63108, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20631792" target="_blank"〉PubMed〈/a〉
    Keywords: Anaerobiosis ; Bacteria/classification/genetics/isolation & purification/metabolism ; Bacteriophages/classification/enzymology/genetics/isolation & purification ; DNA, Viral/analysis/genetics ; Feces/*microbiology/*virology ; Female ; Genes, Bacterial/genetics ; Genome, Bacterial/genetics ; Genome, Viral/genetics ; Heredity/genetics ; Humans ; Intestines/microbiology/virology ; *Metagenome/genetics ; *Mothers ; Prophages/classification/genetics/isolation & purification ; RNA, Ribosomal, 16S/analysis/genetics ; Sequence Analysis, DNA ; Time Factors ; *Twins, Monozygotic/genetics ; Viral Proteins/analysis/genetics/metabolism ; Viruses/classification/*genetics/*isolation & purification
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 4
    facet.materialart.
    Unknown
    CCR5 is a receptor for Staphylococcus aureus leukotoxin ED (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-12-14
    Description: Pore-forming toxins are critical virulence factors for many bacterial pathogens and are central to Staphylococcus aureus-mediated killing of host cells. S. aureus encodes pore-forming bi-component leukotoxins that are toxic towards neutrophils, but also specifically target other immune cells. Despite decades since the first description of staphylococcal leukocidal activity, the host factors responsible for the selectivity of leukotoxins towards different immune cells remain unknown. Here we identify the human immunodeficiency virus (HIV) co-receptor CCR5 as a cellular determinant required for cytotoxic targeting of subsets of myeloid cells and T lymphocytes by the S. aureus leukotoxin ED (LukED). We further demonstrate that LukED-dependent cell killing is blocked by CCR5 receptor antagonists, including the HIV drug maraviroc. Remarkably, CCR5-deficient mice are largely resistant to lethal S. aureus infection, highlighting the importance of CCR5 targeting in S. aureus pathogenesis. Thus, depletion of CCR5(+) leukocytes by LukED suggests a new immune evasion mechanism of S. aureus that can be therapeutically targeted.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3536884/" 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/PMC3536884/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Alonzo, Francis 3rd -- Kozhaya, Lina -- Rawlings, Stephen A -- Reyes-Robles, Tamara -- DuMont, Ashley L -- Myszka, David G -- Landau, Nathaniel R -- Unutmaz, Derya -- Torres, Victor J -- F32 AI098395/AI/NIAID NIH HHS/ -- R01 AI065303/AI/NIAID NIH HHS/ -- R01-AI065303/AI/NIAID NIH HHS/ -- R21 AI087973/AI/NIAID NIH HHS/ -- R21-AI087973/AI/NIAID NIH HHS/ -- R42-MH084372-02A1/MH/NIMH NIH HHS/ -- R56-AI091856-01A1/AI/NIAID NIH HHS/ -- England -- Nature. 2013 Jan 3;493(7430):51-5. doi: 10.1038/nature11724. Epub 2012 Dec 12.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, New York University School of Medicine, New York, New York 10016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23235831" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacterial Toxins/*metabolism ; CCR5 Receptor Antagonists ; Cell Death ; Cells, Cultured ; Dendritic Cells/cytology/immunology/metabolism ; Exotoxins/*metabolism ; Female ; Humans ; Immune Evasion ; Immunologic Memory ; Jurkat Cells ; Mice ; Myeloid Cells/cytology/immunology/metabolism ; Receptors, CCR5/*metabolism ; Staphylococcus aureus/immunology/*pathogenicity ; T-Lymphocytes/cytology/immunology/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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 5
    facet.materialart.
    Unknown
    Activation of the innate immune receptor Dectin-1 upon formation of a 'phagocytic synapse' (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-04-29
    Description: Innate immune cells must be able to distinguish between direct binding to microbes and detection of components shed from the surface of microbes located at a distance. Dectin-1 (also known as CLEC7A) is a pattern-recognition receptor expressed by myeloid phagocytes (macrophages, dendritic cells and neutrophils) that detects beta-glucans in fungal cell walls and triggers direct cellular antimicrobial activity, including phagocytosis and production of reactive oxygen species (ROS). In contrast to inflammatory responses stimulated upon detection of soluble ligands by other pattern-recognition receptors, such as Toll-like receptors (TLRs), these responses are only useful when a cell comes into direct contact with a microbe and must not be spuriously activated by soluble stimuli. In this study we show that, despite its ability to bind both soluble and particulate beta-glucan polymers, Dectin-1 signalling is only activated by particulate beta-glucans, which cluster the receptor in synapse-like structures from which regulatory tyrosine phosphatases CD45 and CD148 (also known as PTPRC and PTPRJ, respectively) are excluded (Supplementary Fig. 1). The 'phagocytic synapse' now provides a model mechanism by which innate immune receptors can distinguish direct microbial contact from detection of microbes at a distance, thereby initiating direct cellular antimicrobial responses only when they are required.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3084546/" 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/PMC3084546/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodridge, Helen S -- Reyes, Christopher N -- Becker, Courtney A -- Katsumoto, Tamiko R -- Ma, Jun -- Wolf, Andrea J -- Bose, Nandita -- Chan, Anissa S H -- Magee, Andrew S -- Danielson, Michael E -- Weiss, Arthur -- Vasilakos, John P -- Underhill, David M -- AI066120/AI/NIAID NIH HHS/ -- AI071116/AI/NIAID NIH HHS/ -- R01 AI066120/AI/NIAID NIH HHS/ -- R01 AI066120-05/AI/NIAID NIH HHS/ -- R01 AI071116/AI/NIAID NIH HHS/ -- R01 AI071116-04/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Apr 28;472(7344):471-5. doi: 10.1038/nature10071.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IBD and Immunobiology Research Institute, 8700 Beverly Boulevard, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21525931" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD45/deficiency/metabolism ; Cell Wall/chemistry/immunology ; Cells, Cultured ; Humans ; Immunity, Innate/*immunology ; Immunological Synapses/*immunology ; Lectins, C-Type ; Macrophages/immunology ; Membrane Proteins/deficiency/genetics/*immunology ; Mice ; *Models, Immunological ; Nerve Tissue Proteins/deficiency/genetics/*immunology ; Phagocytosis/*immunology ; Reactive Oxygen Species/metabolism ; Receptor-Like Protein Tyrosine Phosphatases, Class 3/deficiency/metabolism ; Saccharomyces cerevisiae/chemistry/immunology ; Signal Transduction/immunology ; Solubility ; beta-Glucans/chemistry/immunology
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 6
    facet.materialart.
    Unknown
    A tumour suppressor network relying on the polyamine-hypusine axis (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-06-23
    Description: Tumour suppressor genes encode a broad class of molecules whose mutational attenuation contributes to malignant progression. In the canonical situation, the tumour suppressor is completely inactivated through a two-hit process involving a point mutation in one allele and chromosomal deletion of the other. Here, to identify tumour suppressor genes in lymphoma, we screen a short hairpin RNA library targeting genes deleted in human lymphomas. We functionally identify those genes whose suppression promotes tumorigenesis in a mouse lymphoma model. Of the nine tumour suppressors we identified, eight correspond to genes occurring in three physically linked 'clusters', suggesting that the common occurrence of large chromosomal deletions in human tumours reflects selective pressure to attenuate multiple genes. Among the new tumour suppressors are adenosylmethionine decarboxylase 1 (AMD1) and eukaryotic translation initiation factor 5A (eIF5A), two genes associated with hypusine, a unique amino acid produced as a product of polyamine metabolism through a highly conserved pathway. Through a secondary screen surveying the impact of all polyamine enzymes on tumorigenesis, we establish the polyamine-hypusine axis as a new tumour suppressor network regulating apoptosis. Unexpectedly, heterozygous deletions encompassing AMD1 and eIF5A often occur together in human lymphomas and co-suppression of both genes promotes lymphomagenesis in mice. Thus, some tumour suppressor functions can be disabled through a two-step process targeting different genes acting in the same pathway.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3530829/" 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/PMC3530829/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Scuoppo, Claudio -- Miething, Cornelius -- Lindqvist, Lisa -- Reyes, Jose -- Ruse, Cristian -- Appelmann, Iris -- Yoon, Seungtai -- Krasnitz, Alexander -- Teruya-Feldstein, Julie -- Pappin, Darryl -- Pelletier, Jerry -- Lowe, Scott W -- CA087497/CA/NCI NIH HHS/ -- CA148532/CA/NCI NIH HHS/ -- MOP-106530/Canadian Institutes of Health Research/Canada -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA087497/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2012 Jul 12;487(7406):244-8. doi: 10.1038/nature11126.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Watson School of Biological Sciences, Cold Spring Harbor Laboratory, New York 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22722845" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor ; Disease Models, Animal ; Female ; Gene Deletion ; Gene Regulatory Networks ; Genetic Testing ; Humans ; Lymphoma, B-Cell/*genetics/physiopathology ; Lysine/*analogs & derivatives/chemistry ; Mice ; Mice, Inbred C57BL ; Polyamines/*chemistry ; RNA, Small Interfering/genetics/metabolism ; Reproducibility of Results ; Tumor Suppressor Proteins/*genetics
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 7
    facet.materialart.
    Unknown
    Live attenuated malaria vaccine designed to protect through hepatic CD8(+) T cell immunity (2011)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2011-09-10
    Description: Our goal is to develop a vaccine that sustainably prevents Plasmodium falciparum (Pf) malaria in 〉/=80% of recipients. Pf sporozoites (PfSPZ) administered by mosquito bites are the only immunogens shown to induce such protection in humans. Such protection is thought to be mediated by CD8(+) T cells in the liver that secrete interferon-gamma (IFN-gamma). We report that purified irradiated PfSPZ administered to 80 volunteers by needle inoculation in the skin was safe, but suboptimally immunogenic and protective. Animal studies demonstrated that intravenous immunization was critical for inducing a high frequency of PfSPZ-specific CD8(+), IFN-gamma-producing T cells in the liver (nonhuman primates, mice) and conferring protection (mice). Our results suggest that intravenous administration of this vaccine will lead to the prevention of infection with Pf malaria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Epstein, J E -- Tewari, K -- Lyke, K E -- Sim, B K L -- Billingsley, P F -- Laurens, M B -- Gunasekera, A -- Chakravarty, S -- James, E R -- Sedegah, M -- Richman, A -- Velmurugan, S -- Reyes, S -- Li, M -- Tucker, K -- Ahumada, A -- Ruben, A J -- Li, T -- Stafford, R -- Eappen, A G -- Tamminga, C -- Bennett, J W -- Ockenhouse, C F -- Murphy, J R -- Komisar, J -- Thomas, N -- Loyevsky, M -- Birkett, A -- Plowe, C V -- Loucq, C -- Edelman, R -- Richie, T L -- Seder, R A -- Hoffman, S L -- 5R44AI055229-07/AI/NIAID NIH HHS/ -- 5R44AI058375-05/AI/NIAID NIH HHS/ -- 5R44AI058499-05/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Oct 28;334(6055):475-80. doi: 10.1126/science.1211548. Epub 2011 Sep 8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉U.S. Military Malaria Vaccine Program, Naval Medical Research Center, Silver Spring, MD 20910, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21903775" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Animals ; Antibodies, Protozoan/blood/immunology ; Antigens, Protozoan/immunology ; CD8-Positive T-Lymphocytes/*immunology ; Humans ; Injections, Intravenous ; Injections, Subcutaneous ; Interferon-gamma/biosynthesis/immunology ; Liver/*immunology ; Macaca mulatta ; Malaria Vaccines/administration & dosage/adverse effects/*immunology ; Malaria, Falciparum/*prevention & control ; Mice ; Middle Aged ; Plasmodium falciparum/*immunology ; Rabbits ; Sporozoites/*immunology ; Vaccines, Attenuated/administration & dosage/adverse effects/immunology ; Young Adult
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 8
    facet.materialart.
    Unknown
    Interactions between commensal fungi and the C-type lectin receptor Dectin-1 influence colitis (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-08
    Description: The intestinal microflora, typically equated with bacteria, influences diseases such as obesity and inflammatory bowel disease. Here, we show that the mammalian gut contains a rich fungal community that interacts with the immune system through the innate immune receptor Dectin-1. Mice lacking Dectin-1 exhibited increased susceptibility to chemically induced colitis, which was the result of altered responses to indigenous fungi. In humans, we identified a polymorphism in the gene for Dectin-1 (CLEC7A) that is strongly linked to a severe form of ulcerative colitis. Together, our findings reveal a eukaryotic fungal community in the gut (the "mycobiome") that coexists with bacteria and substantially expands the repertoire of organisms interacting with the intestinal immune system to influence health and disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3432565/" 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/PMC3432565/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iliev, Iliyan D -- Funari, Vincent A -- Taylor, Kent D -- Nguyen, Quoclinh -- Reyes, Christopher N -- Strom, Samuel P -- Brown, Jordan -- Becker, Courtney A -- Fleshner, Phillip R -- Dubinsky, Marla -- Rotter, Jerome I -- Wang, Hanlin L -- McGovern, Dermot P B -- Brown, Gordon D -- Underhill, David M -- 086558/Wellcome Trust/United Kingdom -- AI071116/AI/NIAID NIH HHS/ -- P01-DK046763/DK/NIDDK NIH HHS/ -- R01 DK093426/DK/NIDDK NIH HHS/ -- UL1 RR033176/RR/NCRR NIH HHS/ -- UL1 TR000124/TR/NCATS NIH HHS/ -- UL1RR033176/RR/NCRR NIH HHS/ -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Jun 8;336(6086):1314-7. doi: 10.1126/science.1221789. Epub 2012 Jun 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inflammatory Bowel and Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22674328" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Fungal/blood ; Candida tropicalis/immunology/isolation & purification/pathogenicity/physiology ; Colitis, Ulcerative/chemically induced/*immunology/*microbiology ; Colon/immunology/*microbiology ; Colony Count, Microbial ; Dextran Sulfate ; Disease Susceptibility ; Female ; Fungi/classification/*immunology/isolation & purification/*physiology ; Haplotypes ; Humans ; Immunity, Innate ; Immunity, Mucosal ; Intestinal Mucosa/immunology/*microbiology ; Intestines/immunology/microbiology ; Lectins, C-Type/deficiency/*genetics/*metabolism ; Metagenome ; Mice ; Mice, Inbred C57BL ; Polymorphism, Single Nucleotide
    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)
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    PAPER CURRENT
  • 9
    facet.materialart.
    Unknown
    Monitoring for Renal Stone Recurrence in Astronauts With History of Stone (2014)
    In:  CASI
    Details
    Publication Date: 2019-07-19
    Description: After an initial stone episode persons are at increased risk for future stone formation. A systematic approach is required to monitor the efficacy of treatment and preventive measures, and to assess the risk of developing new stones. This is important for persons working in critical jobs or austere environments, such as astronauts. A literature review of the current standards of care for renal stone monitoring and imaging was done. Military and civil aviation standards were also reviewed, as well as the medical precedents from the space program. Additionally, a new, more effective, renal stone ultrasound protocol has been developed. Using this work, a monitoring algorithm was proposed that takes into consideration the unique mission and operational environment of spaceflight. The approach to imaging persons with history of renal stones varies widely in the literature. Imaging is often done yearly or biannually, which may be too long for mission critical personnel. In the proposed algorithm astronauts with a history of renal stone, who may be under consideration for assignment, are imaged by a detailed, physiciandriven, ultrasound protocol. Unassigned personnel are monitored by yearly ultrasound and urine studies. Any positive ultrasound study is then followed by low-dose renal computed tomography scan. Other criteria are also established. The proposed algorithm provides a balanced approach between efficacy and reduced radiation exposure for the monitoring of astronauts with a renal stone history. This may eventually allow a transition from a risk-averse, to a risk-modifying approach that can enable continued service of individuals with history of renal stone that have adequately controlled risk factors.
    Keywords: Aerospace Medicine
    Type: JSC-CN-29923 , Aerospace Medical Association Annual Scientific Meeting; May 11, 2014 - May 15, 2014; San Diego, CA; United States
    Format: application/pdf
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
  • 10
    facet.materialart.
    Unknown
    A Guideline for the Management of Renal Stones in Astronauts (2014)
    In:  CASI
    Details
    Publication Date: 2019-07-19
    Description: There are no specific guidelines for the management of renal stones in astronauts. Given the increased risk for bone loss, hypercalcuria, and stone formation due to microgravity, a clinical practice guideline is needed. Methods An extensive review of the literature and current aeromedical standards for the management of renal stones was done. The NASA Flight Medicine Clinic's electronic medical record and Longitudinal Survey of Astronaut Health were also reviewed. This information was used to create an algorithm for the management of renal stones in astronauts. Results Guidelines are proposed based on accepted standards of care, with consideration to the environment of spaceflight. In a usual medical setting, asymptomatic, small stones less than 7 mm are often observed over time. Given the constraints of schedule, and the risks to crew health and mission, this approach is too liberal. An upper limit of 3 mm stone diameter was adopted before requiring intervention, because this is the largest size that has a significant chance of spontaneous passage on its own. Other specific guidelines were also created. Discussion The spaceflight environment requires more aggressive treatment than would otherwise be found with the usual practice of medicine. A small stone can become a major problem because it may ultimately require medical evacuation from orbit. Thus renal stones are a significant mission threat and should be managed in a systematic way to mitigate risks to crew health and mission success.
    Keywords: Aerospace Medicine
    Type: JSC-CN-29905 , Annual Scientific Meeting of the Aerospace Medical Association; May 11, 2014 - May 15, 2014; San Diego, CA; United States
    Format: application/pdf
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
    NASA TECHNICAL REPORTS
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...