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  • Pregnancy
  • American Association for the Advancement of Science (AAAS)  (41)
  • Annual Reviews
  • 2005-2009  (7)
  • 1980-1984  (27)
  • 1975-1979  (7)
  • 1965-1969
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  • 1
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    Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-04-08
    Description: Aortic aneurysm and dissection are manifestations of Marfan syndrome (MFS), a disorder caused by mutations in the gene that encodes fibrillin-1. Selected manifestations of MFS reflect excessive signaling by the transforming growth factor-beta (TGF-beta) family of cytokines. We show that aortic aneurysm in a mouse model of MFS is associated with increased TGF-beta signaling and can be prevented by TGF-beta antagonists such as TGF-beta-neutralizing antibody or the angiotensin II type 1 receptor (AT1) blocker, losartan. AT1 antagonism also partially reversed noncardiovascular manifestations of MFS, including impaired alveolar septation. These data suggest that losartan, a drug already in clinical use for hypertension, merits investigation as a therapeutic strategy for patients with MFS and has the potential to prevent the major life-threatening manifestation of this disorder.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1482474/" 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/PMC1482474/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habashi, Jennifer P -- Judge, Daniel P -- Holm, Tammy M -- Cohn, Ronald D -- Loeys, Bart L -- Cooper, Timothy K -- Myers, Loretha -- Klein, Erin C -- Liu, Guosheng -- Calvi, Carla -- Podowski, Megan -- Neptune, Enid R -- Halushka, Marc K -- Bedja, Djahida -- Gabrielson, Kathleen -- Rifkin, Daniel B -- Carta, Luca -- Ramirez, Francesco -- Huso, David L -- Dietz, Harry C -- K08 HL067056/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2006 Apr 7;312(5770):117-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16601194" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Antagonists/administration & dosage/therapeutic use ; Angiotensin II Type 1 Receptor Blockers/administration & dosage/*therapeutic use ; Animals ; Antibodies/immunology ; Aorta/pathology ; Aortic Aneurysm/etiology/*prevention & control ; *Disease Models, Animal ; Elastic Tissue/pathology ; Female ; Losartan/administration & dosage/*therapeutic use ; Lung/pathology ; Lung Diseases/drug therapy/pathology ; Marfan Syndrome/complications/*drug therapy/metabolism/pathology ; Mice ; Microfilament Proteins/genetics ; Mutation ; Neutralization Tests ; Pregnancy ; Pregnancy Complications/drug therapy ; Propranolol/administration & dosage/therapeutic use ; Pulmonary Alveoli/pathology ; Receptor, Angiotensin, Type 1/metabolism ; Signal Transduction ; Transforming Growth Factor beta/antagonists & inhibitors/immunology/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Maternal alloantigens promote the development of tolerogenic fetal regulatory T cells in utero (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-12-06
    Description: As the immune system develops, T cells are selected or regulated to become tolerant of self antigens and reactive against foreign antigens. In mice, the induction of such tolerance is thought to be attributable to the deletion of self-reactive cells. Here, we show that the human fetal immune system takes advantage of an additional mechanism: the generation of regulatory T cells (Tregs) that suppress fetal immune responses. We find that substantial numbers of maternal cells cross the placenta to reside in fetal lymph nodes, inducing the development of CD4+CD25highFoxP3+ Tregs that suppress fetal antimaternal immunity and persist at least until early adulthood. These findings reveal a form of antigen-specific tolerance in humans, induced in utero and probably active in regulating immune responses after birth.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2648820/" 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/PMC2648820/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mold, Jeff E -- Michaelsson, Jakob -- Burt, Trevor D -- Muench, Marcus O -- Beckerman, Karen P -- Busch, Michael P -- Lee, Tzong-Hae -- Nixon, Douglas F -- McCune, Joseph M -- AI40312/AI/NIAID NIH HHS/ -- AI68498/AI/NIAID NIH HHS/ -- DP1 OD000329/OD/NIH HHS/ -- DP1 OD000329-01/OD/NIH HHS/ -- DP1 OD000329-02/OD/NIH HHS/ -- DP1 OD000329-03/OD/NIH HHS/ -- DP1 OD000329-04/OD/NIH HHS/ -- HD00850/HD/NICHD NIH HHS/ -- HL083388/HL/NHLBI NIH HHS/ -- OD000329/OD/NIH HHS/ -- R01 HL083388/HL/NHLBI NIH HHS/ -- R01 HL083388-02/HL/NHLBI NIH HHS/ -- R37 AI040312/AI/NIAID NIH HHS/ -- R37 AI040312-09/AI/NIAID NIH HHS/ -- R37 AI040312-10/AI/NIAID NIH HHS/ -- R37 AI040312-11/AI/NIAID NIH HHS/ -- R37 AI040312-12/AI/NIAID NIH HHS/ -- R37 AI040312-13/AI/NIAID NIH HHS/ -- RR024131/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2008 Dec 5;322(5907):1562-5. doi: 10.1126/science.1164511.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Experimental Medicine, Department of Medicine, University of California at San Francisco (UCSF), San Francisco, CA 94110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19056990" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Antigen-Presenting Cells/immunology ; Cells, Cultured ; Child ; Chimerism ; Female ; Fetus/*immunology ; Forkhead Transcription Factors/metabolism ; Gene Expression Profiling ; Humans ; *Immune Tolerance ; Isoantigens/*immunology ; Lymph Nodes/cytology/*immunology ; Lymphocyte Activation ; *Maternal-Fetal Exchange ; Pregnancy ; Self Tolerance ; T-Lymphocytes, Regulatory/*immunology ; Thymus Gland/immunology ; Transforming Growth Factors/genetics/metabolism ; Tumor Necrosis Factors/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Proliferation of functional hair cells in vivo in the absence of the retinoblastoma protein (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: In mammals, hair cell loss causes irreversible hearing and balance impairment because hair cells are terminally differentiated and do not regenerate spontaneously. By profiling gene expression in developing mouse vestibular organs, we identified the retinoblastoma protein (pRb) as a candidate regulator of cell cycle exit in hair cells. Differentiated and functional mouse hair cells with a targeted deletion of Rb1 undergo mitosis, divide, and cycle, yet continue to become highly differentiated and functional. Moreover, acute loss of Rb1 in postnatal hair cells caused cell cycle reentry. Manipulation of the pRb pathway may ultimately lead to mammalian hair cell regeneration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sage, Cyrille -- Huang, Mingqian -- Karimi, Kambiz -- Gutierrez, Gabriel -- Vollrath, Melissa A -- Zhang, Duan-Sun -- Garcia-Anoveros, Jaime -- Hinds, Philip W -- Corwin, Jeffrey T -- Corey, David P -- Chen, Zheng-Yi -- DC-00200/DC/NIDCD NIH HHS/ -- DC-04546/DC/NIDCD NIH HHS/ -- DC-AG20208/DC/NIDCD NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1114-8. Epub 2005 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology Service, MGH-HMS Center for Nervous System Repair, Massachusetts General Hospital and Harvard Medical School, Boston, MA 02114, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653467" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Cell Count ; Cell Cycle ; Cell Differentiation ; *Cell Proliferation ; Cell Shape ; Cochlea/cytology/embryology ; Female ; Gene Deletion ; Gene Expression Profiling ; Genes, Retinoblastoma ; Hair Cells, Auditory, Inner/*cytology/*physiology ; Mice ; Mice, Knockout ; Mitosis ; Oligonucleotide Array Sequence Analysis ; Pregnancy ; Pyridinium Compounds/metabolism ; Quaternary Ammonium Compounds/metabolism ; Regeneration ; Retinoblastoma Protein/genetics/*physiology ; Saccule and Utricle/embryology/metabolism ; Stem Cells/cytology/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 4
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    Dieldrin-induced mortality in an endangered species, the gray bat (Myotis grisescens) (1978)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1978-03-24
    Description: Brains of juvenile gray bats, Myotis grisescens, found dead beneath maternity roosts in two Missouri caves contained lethal concentrations of dieldrin. One colony appeared to be abnormally small, and more dead bats were found a year after the juvenile bats had been collected. This is the first report to link the field mortality of bats directly to insecticide residues acquired through the food chain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clark, D R Jr -- LaVal, R K -- Swineford, D M -- New York, N.Y. -- Science. 1978 Mar 24;199(4335):1357-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/564550" target="_blank"〉PubMed〈/a〉
    Keywords: Aldrin/adverse effects ; Animals ; Body Weight ; Brain Chemistry ; *Chiroptera ; Dieldrin/*adverse effects/analysis ; Environmental Exposure ; Female ; Lactation ; Male ; Missouri ; Pesticide Residues ; Pregnancy
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Dorsal root ganglion neurons are destroyed by exposure in utero to maternal antibody to nerve growth factor (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-11-21
    Description: Rats and guinea pigs, when immunized with mouse nerve growth factor, produce antibodies that cross-react with their own nerve growth factor. The antibodies reach developing offspring of these animals both prenatally (rats and guinea pigs) and postnatally (rats). Depriving the fetus of nerve growth factor in this way results in the destruction of up to 85 percent of dorsal root ganglion neurons as well as destruction of sympathetic neurons. Sensory neurons of placodal origin in the nodose ganglion were not affected. These data demonstrate that dorsal root ganglion neurons go through a phase of nerve growth factor dependence in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johnson, E M Jr -- Gorin, P D -- Brandeis, L D -- Pearson, J -- HD12260/HD/NICHD NIH HHS/ -- HL20604/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1980 Nov 21;210(4472):916-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7192014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibodies ; Female ; Ganglia, Spinal/cytology/*embryology/growth & development ; Guinea Pigs ; Lactation ; Maternal-Fetal Exchange ; Milk/immunology ; Nerve Growth Factors/*immunology ; Pregnancy ; Rats
    Print ISSN: 0036-8075
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  • 6
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    Reduction in oocyte number following prenatal exposure to a diet high in galactose (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-12-04
    Description: When pregnant rats were fed a 50 percent galactose diet there was a striking reduction in oocyte number in the offspring. The most prominent effects were noted after exposure to galactose during the premeiotic stages of oogenesis. Prenatal exposure to galactose or its metabolites may contribute to the premature ovarian failure characteristic of human galactosemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Y T -- Mattison, D R -- Feigenbaum, L -- Fukui, H -- Schulman, J D -- New York, N.Y. -- Science. 1981 Dec 4;214(4525):1145-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7302587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dietary Carbohydrates/*physiology ; Female ; Fetus/drug effects/physiology ; Galactose/*pharmacology ; Maternal-Fetal Exchange ; Oocytes/drug effects/*physiology ; Ovum/*physiology ; Pregnancy ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Male vole urine changes luteinizing hormone-releasing hormone and norepinephrine in female olfactory bulb (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-05-01
    Description: Female prairie voles (Microtus ochrogaster) exposed to a single drop of male urine on the upper lip showed changes in concentrations of luteinizing hormone-releasing hormone (LHRH) and norepinephrine in olfactory bulb tissue; no such changes occurred in dopamine concentration. The changes were measured in the posterior but not the anterior olfactory bulb tissue of females within 1 hour after they were exposed to urine. These females also showed rapid increases in serum concentrations of luteinizing hormone. Females exposed to water on the upper lip showed none of these changes. These results suggest that in this species LHRH and norepinephrine in the olfactory bulb may mediate luteinizing hormone release in response to external (pheromonal) chemical cues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dluzen, D E -- Ramirez, V D -- Carter, C S -- Getz, L L -- HDO9328/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1981 May 1;212(4494):573-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7010608" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arvicolinae/*physiology ; Estrus ; Female ; Gonadotropin-Releasing Hormone/*metabolism ; Humans ; Luteinizing Hormone/blood ; Male ; Norepinephrine/*metabolism ; Olfactory Bulb/*metabolism ; Pheromones/*urine ; Pregnancy ; Reproduction ; Rodentia/*physiology ; Stress, Psychological/physiopathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Associative learning in premature hydranencephalic and normal twins (1980)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1980-11-28
    Description: A hydranencephalic infant lacking cerebral hemispheres and a normal twin were tested for associative learning. After repeated trials in which two stimuli were temporally paired, test trials were given in which the second stimulus was omitted. Cardiac orienting responses to stimulus omission indicated that learning had taken place in both infants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tuber, D S -- Berntson, G G -- Bachman, D S -- Allen, J N -- New York, N.Y. -- Science. 1980 Nov 28;210(4473):1035-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7192015" target="_blank"〉PubMed〈/a〉
    Keywords: Anencephaly/*physiopathology ; Association/*physiology ; Behavior/physiology ; Brain/physiology ; Brain Stem/physiology ; Female ; Heart Rate ; Humans ; Hydranencephaly/*physiopathology ; Infant ; Infant, Newborn ; Infant, Premature/*psychology ; Male ; Pregnancy ; Twins, Dizygotic
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Stimulation of prostaglandin biosynthesis by urine of the human fetus may serve as a trigger for parturition (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-29
    Description: Urine of the human fetus stimulated prostaglandin biosynthesis in vitro by increasing the conversion of arachidonic acid into prostaglandins. The stimulatory activity in urine from fetuses delivered at term after labor of spontaneous onset was greater than that in urine from fetuses delivered by cesarean section at term before the onset of labor. Such stimulation of prostaglandin biosynthesis by the fetal membranes, by way of a substance released into the urine and thence into amniotic fluid, could serve as a signal for the initiation of parturition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strickland, D M -- Saeed, S A -- Casey, M L -- Mitchell, M D -- 5-P50-HD11149/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):521-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6573023" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Dinoprostone ; Extraembryonic Membranes/physiology ; Female ; Fetus/*physiology ; Humans ; *Labor Onset ; *Labor, Obstetric ; Male ; Pregnancy ; Prostaglandins/*biosynthesis ; Prostaglandins E/biosynthesis ; *Urine
    Print ISSN: 0036-8075
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  • 10
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    Multiple causes of high extinction risk in large mammal species (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-23
    Description: Many large animal species have a high risk of extinction. This is usually thought to result simply from the way that species traits associated with vulnerability, such as low reproductive rates, scale with body size. In a broad-scale analysis of extinction risk in mammals, we find two additional patterns in the size selectivity of extinction risk. First, impacts of both intrinsic and environmental factors increase sharply above a threshold body mass around 3 kilograms. Second, whereas extinction risk in smaller species is driven by environmental factors, in larger species it is driven by a combination of environmental factors and intrinsic traits. Thus, the disadvantages of large size are greater than generally recognized, and future loss of large mammal biodiversity could be far more rapid than expected.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cardillo, Marcel -- Mace, Georgina M -- Jones, Kate E -- Bielby, Jon -- Bininda-Emonds, Olaf R P -- Sechrest, Wes -- Orme, C David L -- Purvis, Andy -- New York, N.Y. -- Science. 2005 Aug 19;309(5738):1239-41. Epub 2005 Jul 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, Imperial College London, Silwood Park, Ascot SL5 7PY, UK. m.cardillo@imperial.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16037416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biodiversity ; Biological Evolution ; *Body Size ; Body Weight ; Conservation of Natural Resources ; *Ecosystem ; *Environment ; Female ; Homing Behavior ; Humans ; *Mammals/physiology ; Models, Biological ; Models, Statistical ; Population Density ; Population Dynamics ; Pregnancy ; Pregnancy, Animal ; Regression Analysis ; Risk ; Weaning
    Print ISSN: 0036-8075
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