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  • Aerospace Medicine  (3)
  • Age determination
  • Biological data
  • Mice, Inbred C57BL
  • 2010-2014  (5)
  • 1995-1999  (1)
  • 1
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    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)
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  • 2
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    Severe stress switches CRF action in the nucleus accumbens from appetitive to aversive (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-09-21
    Description: Stressors motivate an array of adaptive responses ranging from 'fight or flight' to an internal urgency signal facilitating long-term goals. However, traumatic or chronic uncontrollable stress promotes the onset of major depressive disorder, in which acute stressors lose their motivational properties and are perceived as insurmountable impediments. Consequently, stress-induced depression is a debilitating human condition characterized by an affective shift from engagement of the environment to withdrawal. An emerging neurobiological substrate of depression and associated pathology is the nucleus accumbens, a region with the capacity to mediate a diverse range of stress responses by interfacing limbic, cognitive and motor circuitry. Here we report that corticotropin-releasing factor (CRF), a neuropeptide released in response to acute stressors and other arousing environmental stimuli, acts in the nucleus accumbens of naive mice to increase dopamine release through coactivation of the receptors CRFR1 and CRFR2. Remarkably, severe-stress exposure completely abolished this effect without recovery for at least 90 days. This loss of CRF's capacity to regulate dopamine release in the nucleus accumbens is accompanied by a switch in the reaction to CRF from appetitive to aversive, indicating a diametric change in the emotional response to acute stressors. Thus, the current findings offer a biological substrate for the switch in affect which is central to stress-induced depressive disorders.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3475726/" 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/PMC3475726/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lemos, Julia C -- Wanat, Matthew J -- Smith, Jeffrey S -- Reyes, Beverly A S -- Hollon, Nick G -- Van Bockstaele, Elisabeth J -- Chavkin, Charles -- Phillips, Paul E M -- F31 MH086269/MH/NIMH NIH HHS/ -- F31-MH086269/MH/NIMH NIH HHS/ -- F32-DA026273/DA/NIDA NIH HHS/ -- K05 DA020570/DA/NIDA NIH HHS/ -- R01 DA009082/DA/NIDA NIH HHS/ -- R01 DA016782/DA/NIDA NIH HHS/ -- R01 DA030074/DA/NIDA NIH HHS/ -- R01 MH079292/MH/NIMH NIH HHS/ -- R01-DA009082/DA/NIDA NIH HHS/ -- R01-DA016782/DA/NIDA NIH HHS/ -- R01-DA030074/DA/NIDA NIH HHS/ -- R01-MH079292/MH/NIMH NIH HHS/ -- England -- Nature. 2012 Oct 18;490(7420):402-6. doi: 10.1038/nature11436. Epub 2012 Sep 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle, Washington 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22992525" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Appetitive Behavior/drug effects/*physiology ; Avoidance Learning/drug effects/*physiology ; Corticotropin-Releasing Hormone/*metabolism/pharmacology ; Dopamine/metabolism/secretion ; Male ; Mice ; Mice, Inbred C57BL ; Nucleus Accumbens/*metabolism/physiopathology ; Receptors, Corticotropin-Releasing Hormone/agonists/antagonists & ; inhibitors/deficiency/metabolism ; Signal Transduction/drug effects ; Stress, Psychological/*metabolism/physiopathology
    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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  • 3
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    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)
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  • 4
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    Marked Exacerbation of Orthostatic Intolerance After Long vs. Short-Duration Spaceflight in Veteran Astronauts (1999)
    In:  Other Sources
    Details
    Publication Date: 2019-07-17
    Description: The incidence of postflight orthostatic intolerance following short-duration spaceflight is about 20%. However, the incidence following long-duration spaceflight is unknown. We performed tilt tests on six astronauts before and after their long-duration (129 - 190 days) spaceflights and compared these data to those obtained during stand tests before and after their previous short-duration missions and also to tilt test data from 20 different short-duration (8 - 16 days) flight astronauts. Five of these six became presyncopal during tilt testing after long-duration flights: only one had become presyncopal during stand testing after short-duration flights. Five of the twenty astronauts who flew on other short-duration flights, became presyncopal during upright tilt on landing day. Long-duration presyncopal subjects had lower stroke volumes, lower cardiac outputs and higher peripheral vascular resistance than short-duration presyncopal subjects, but their heart rate responses were not different. One subject had subnormal norepinephrine release with upright posture after a long but not short flight. Plasma volume losses were not greater after long flights. Long-duration spaceflight markedly increases orthostatic intolerance, probably related to altered autonomic function.
    Keywords: Aerospace Medicine
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  • 5
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    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
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  • 6
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    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
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