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  • 1
    Publication Date: 1991-12-20
    Description: In the mollusk Aplysia the neurotransmitter serotonin (5HT) has a fundamental modulatory role in several forms of learning and memory that involve an increase in the efficacy of synaptic transmission between tail sensory neurons (SNs) and motor neurons. The classical 5HT antagonist cyproheptadine (CYP) permits dissociation of three forms of serotonergic modulation in these SNs: (i) CYP reversibly blocks spike-broadening induced either by exogenous application of 5HT or by sensitizing stimulation of a tail nerve. (ii) CYP does not block 5HT-induced or tail input-induced increases in SN somatic excitability. (iii) Concomitant with its block of spike-broadening, CYP reversibly blocks 5HT-induced facilitation of synaptic transmission from SNs. These results suggest that endogenously released 5HT may act at different receptor subtypes that are coupled to different forms of neuromodulation in tail SNs of Aplysia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mercer, A R -- Emptage, N J -- Carew, T J -- MH 141083/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1991 Dec 20;254(5039):1811-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Yale University, Department of Psychology, New Haven, CT 06520.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1662413" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Aplysia ; Cyproheptadine/*pharmacology ; Evoked Potentials/drug effects ; In Vitro Techniques ; Models, Neurological ; Motor Neurons/physiology ; Neurons, Afferent/drug effects/*physiology ; Serotonin/*pharmacology ; Synapses/drug effects/*physiology ; Synaptic Transmission/drug effects
    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
    Publication Date: 1991-07-12
    Description: Effects of infections by the ciliate Lambornella clarki on larval populations of its mosquito host Aedes sierrensis were examined in laboratory and field studies. When host populations developed with sufficient food, mortality from parasites was additive and reduced the number of emerging mosquitoes. For food-limited populations, mortality was compensatory or depensatory; emerging adults were as or more abundant with higher average fitness than those from uninfected control populations. When nutrients were scarce, parasitic infections relaxed larval competition and increased per capita food by reducing host abundance. Food limitation altered larval feeding behavior, reducing horizontal transmission and subsequent mortality from parasitism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Washburn, J O -- Mercer, D R -- Anderson, J R -- AI20245/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1991 Jul 12;253(5016):185-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Entomology, University of California, Berkeley 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/1906637" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*parasitology/physiology ; Animals ; Ciliophora/*physiology ; Ecology ; Population Dynamics ; Trees
    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
    Publication Date: 2009-01-03
    Description: We report abundant nanodiamonds in sediments dating to 12.9 +/- 0.1 thousand calendar years before the present at multiple locations across North America. Selected area electron diffraction patterns reveal two diamond allotropes in this boundary layer but not above or below that interval. Cubic diamonds form under high temperature-pressure regimes, and n-diamonds also require extraordinary conditions, well outside the range of Earth's typical surficial processes but common to cosmic impacts. N-diamond concentrations range from approximately 10 to 3700 parts per billion by weight, comparable to amounts found in known impact layers. These diamonds provide strong evidence for Earth's collision with a rare swarm of carbonaceous chondrites or comets at the onset of the Younger Dryas cool interval, producing multiple airbursts and possible surface impacts, with severe repercussions for plants, animals, and humans in North America.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kennett, D J -- Kennett, J P -- West, A -- Mercer, C -- Hee, S S Que -- Bement, L -- Bunch, T E -- Sellers, M -- Wolbach, W S -- New York, N.Y. -- Science. 2009 Jan 2;323(5910):94. doi: 10.1126/science.1162819.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anthropology, University of Oregon, Eugene, OR 97403, USA. dkennett@uoregon.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19119227" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Diamond ; Extinction, Biological ; *Geologic Sediments ; *Meteoroids ; Microscopy, Electron, Scanning Transmission ; Nanostructures ; North America ; Time
    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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  • 4
    Publication Date: 2009-12-19
    Description: Acute exposure to ionizing radiation can cause lethal damage to the gastrointestinal (GI) tract, a condition called the GI syndrome. Whether the target cells affected by radiation to cause the GI syndrome are derived from the epithelium or endothelium and whether the target cells die by apoptosis or other mechanisms are controversial issues. Studying mouse models, we found that selective deletion of the proapoptotic genes Bak1 and Bax from the GI epithelium or from endothelial cells did not protect mice from developing the GI syndrome after sub-total-body gamma irradiation. In contrast, selective deletion of p53 from the GI epithelium, but not from endothelial cells, sensitized irradiated mice to the GI syndrome. Transgenic mice overexpressing p53 in all tissues were protected from the GI syndrome after irradiation. These results suggest that the GI syndrome is caused by the death of GI epithelial cells and that these epithelial cells die by a mechanism that is regulated by p53 but independent of apoptosis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2897160/" 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/PMC2897160/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kirsch, David G -- Santiago, Philip M -- di Tomaso, Emmanuelle -- Sullivan, Julie M -- Hou, Wu-Shiun -- Dayton, Talya -- Jeffords, Laura B -- Sodha, Pooja -- Mercer, Kim L -- Cohen, Rhianna -- Takeuchi, Osamu -- Korsmeyer, Stanley J -- Bronson, Roderick T -- Kim, Carla F -- Haigis, Kevin M -- Jain, Rakesh K -- Jacks, Tyler -- K08 CA 114176/CA/NCI NIH HHS/ -- K08 CA114176/CA/NCI NIH HHS/ -- K08 CA114176-05/CA/NCI NIH HHS/ -- P01 CA080124/CA/NCI NIH HHS/ -- P01 CA080124-01A1/CA/NCI NIH HHS/ -- P01 CA80124/CA/NCI NIH HHS/ -- P30 CA014051/CA/NCI NIH HHS/ -- P30 CA014051-38/CA/NCI NIH HHS/ -- P30 DK043351/DK/NIDDK NIH HHS/ -- P30-CA14051/CA/NCI NIH HHS/ -- RC1 AI078521/AI/NIAID NIH HHS/ -- RC1 AI078521-01/AI/NIAID NIH HHS/ -- RC1-AI078521/AI/NIAID NIH HHS/ -- U19-AI06775/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jan 29;327(5965):593-6. doi: 10.1126/science.1166202. Epub 2009 Dec 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20019247" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Cell Death ; Epithelial Cells/cytology/physiology/radiation effects ; Gamma Rays/*adverse effects ; Gene Deletion ; Genes, p53 ; Intestinal Diseases/etiology/pathology/*physiopathology ; Intestinal Mucosa/pathology/physiopathology/*radiation effects ; Intestine, Small/pathology/physiopathology/*radiation effects ; Mesoderm/cytology ; Mice ; Mice, Transgenic ; Models, Biological ; Radiation Dosage ; Radiation Injuries/etiology/pathology/*physiopathology ; Tumor Suppressor Protein p53/*physiology ; bcl-2 Homologous Antagonist-Killer Protein/genetics/metabolism ; bcl-2-Associated X Protein/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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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 2003-02-22
    Description: By modifying habitats and creating bridges and barriers between landmasses, climate change and tectonic events are believed to have important consequences for diversification of terrestrial organisms. Such consequences should be most evident in phylogenetic histories of groups that are ancient, widespread, and diverse. The squirrel family (Sciuridae) is one of very few mammalian families endemic to Eurasia, Africa, and North and South America and is ideal for examining these issues. Through phylogenetic and molecular-clock analyses, we infer that arrival and diversification of squirrels in Africa, on Sunda Shelf islands, across Beringea, and across the Panamanian isthmus coincide in timing and location with multiple well-documented sea-level, tectonic, and paleontological events. These precise correspondences point to an important role for global change in the diversification of a major group of mammals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mercer, John M -- Roth, V Louise -- New York, N.Y. -- Science. 2003 Mar 7;299(5612):1568-72. Epub 2003 Feb 20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biology Department, Duke University, Durham, NC 27708-0338, USA. jmercer@duke.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595609" target="_blank"〉PubMed〈/a〉
    Keywords: Africa ; Animals ; Asia ; Bayes Theorem ; Biological Evolution ; Body Constitution ; Central America ; DNA, Mitochondrial/genetics ; DNA, Ribosomal/genetics ; *Environment ; Europe ; *Eye Proteins ; Fossils ; Geography ; Geological Phenomena ; Geology ; North America ; *Phylogeny ; Retinol-Binding Proteins/genetics ; Sciuridae/anatomy & histology/*classification/*genetics ; Sequence Analysis, DNA ; South America
    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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  • 6
    Publication Date: 2011-02-26
    Description: Pituitary adenylate cyclase-activating polypeptide (PACAP) is known to broadly regulate the cellular stress response. In contrast, it is unclear if the PACAP-PAC1 receptor pathway has a role in human psychological stress responses, such as post-traumatic stress disorder (PTSD). Here we find, in heavily traumatized subjects, a sex-specific association of PACAP blood levels with fear physiology, PTSD diagnosis and symptoms in females. We examined 44 single nucleotide polymorphisms (SNPs) spanning the PACAP (encoded by ADCYAP1) and PAC1 (encoded by ADCYAP1R1) genes, demonstrating a sex-specific association with PTSD. A single SNP in a putative oestrogen response element within ADCYAP1R1, rs2267735, predicts PTSD diagnosis and symptoms in females only. This SNP also associates with fear discrimination and with ADCYAP1R1 messenger RNA expression in human brain. Methylation of ADCYAP1R1 in peripheral blood is also associated with PTSD. Complementing these human data, ADCYAP1R1 mRNA is induced with fear conditioning or oestrogen replacement in rodent models. These data suggest that perturbations in the PACAP-PAC1 pathway are involved in abnormal stress responses underlying PTSD. These sex-specific effects may occur via oestrogen regulation of ADCYAP1R1. PACAP levels and ADCYAP1R1 SNPs may serve as useful biomarkers to further our mechanistic understanding of PTSD.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3046811/" 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/PMC3046811/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ressler, Kerry J -- Mercer, Kristina B -- Bradley, Bekh -- Jovanovic, Tanja -- Mahan, Amy -- Kerley, Kimberly -- Norrholm, Seth D -- Kilaru, Varun -- Smith, Alicia K -- Myers, Amanda J -- Ramirez, Manuel -- Engel, Anzhelika -- Hammack, Sayamwong E -- Toufexis, Donna -- Braas, Karen M -- Binder, Elisabeth B -- May, Victor -- AG034504/AG/NIA NIH HHS/ -- DA019624/DA/NIDA NIH HHS/ -- HD27468/HD/NICHD NIH HHS/ -- M01RR00039/RR/NCRR NIH HHS/ -- MH071537/MH/NIMH NIH HHS/ -- P20RR16435/RR/NCRR NIH HHS/ -- R01 AG034504/AG/NIA NIH HHS/ -- R01 HD027468/HD/NICHD NIH HHS/ -- R01 HD027468-13/HD/NICHD NIH HHS/ -- UL1 TR000454/TR/NCATS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Feb 24;470(7335):492-7. doi: 10.1038/nature09856.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Chevy Chase, Maryland 20815, USA. kressle@emory.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21350482" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/metabolism ; Animals ; Conditioning, Classical/physiology ; CpG Islands/genetics ; DNA Methylation ; Estrogens/metabolism/pharmacology ; Fear/physiology ; Female ; Gene Expression Regulation/drug effects ; Genetic Association Studies ; Genetic Predisposition to Disease/*genetics ; Humans ; Male ; Mice ; Pituitary Adenylate Cyclase-Activating Polypeptide/*blood/chemistry ; Polymorphism, Single Nucleotide/genetics ; RNA, Messenger/analysis/biosynthesis/genetics ; Rats ; Receptors, Pituitary Adenylate Cyclase-Activating Polypeptide, Type I/*genetics ; Response Elements/genetics ; Septal Nuclei/drug effects/metabolism ; Sex Characteristics ; Stress Disorders, Post-Traumatic/*blood/*genetics/physiopathology/psychology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 1988-05-27
    Description: Larvae of the treehole mosquito, Aedes sierrensis, release a waterborne factor that induces morphogenesis of one of their prey, the tetrahymenid ciliate Lambornella clarki. Induced free-living trophonts of L. clarki undergo a synchronous response in which cells divide and transform into parasitic cells (theronts) that encyst on larval predators. Parasitic ciliates penetrate the cuticle, enter the hemocoel, and ultimately kill their predator-host. In nature, this trophic shift can lead to predator extinction and dramatic changes in microbial populations. Facultative parasitism by this polymorphic ciliate may have evolved as an antipredator strategy. The experimentally inducible parasitic response of L. clarki provides a novel model for studying cellular morphogenesis of ciliated protozoa.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Washburn, J O -- Gross, M E -- Mercer, D R -- Anderson, J R -- AI20245/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1988 May 27;240(4856):1193-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Entomological Sciences, University of California, Berkely 94720.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3131877" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*parasitology/physiology ; Animals ; Ciliophora/growth & development/*physiology ; Ecology ; Larva ; Predatory Behavior
    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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  • 8
    Publication Date: 2007-07-21
    Description: Queen mandibular pheromone (QMP) has profound effects on dopamine signaling in the brain of young worker honey bees. As dopamine in insects has been strongly implicated in aversive learning, we examined QMP's impact on associative olfactory learning in bees. We found that QMP blocks aversive learning in young workers, but leaves appetitive learning intact. We postulate that QMP's effects on aversive learning enhance the likelihood that young workers remain in close contact with their queen by preventing them from forming an aversion to their mother's pheromone bouquet. The results provide an interesting twist to a story of success and survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vergoz, Vanina -- Schreurs, Haley A -- Mercer, Alison R -- New York, N.Y. -- Science. 2007 Jul 20;317(5836):384-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Zoology, University of Otago, Dunedin, New Zealand.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17641204" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Methoxy-4-hydroxyphenylethanol/pharmacology ; Animals ; Bees/*physiology ; Behavior, Animal/drug effects ; Brain/physiology ; Conditioning (Psychology) ; Cues ; Dopamine/physiology ; Female ; *Learning/drug effects ; Male ; Odors ; Pheromones/chemistry/pharmacology/*physiology ; Reinforcement (Psychology) ; Social Behavior ; Sucrose
    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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  • 9
    Publication Date: 2008-03-29
    Description: The past few years have revealed that the genomes of all studied eukaryotes are almost entirely transcribed, generating an enormous number of non-protein-coding RNAs (ncRNAs). In parallel, it is increasingly evident that many of these RNAs have regulatory functions. Here, we highlight recent advances that illustrate the diversity of ncRNA control of genome dynamics, cell biology, and developmental programming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Amaral, Paulo P -- Dinger, Marcel E -- Mercer, Tim R -- Mattick, John S -- New York, N.Y. -- Science. 2008 Mar 28;319(5871):1787-9. doi: 10.1126/science.1155472.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Bioscience, University of Queensland, St. Lucia QLD 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18369136" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Eukaryotic Cells/*metabolism ; Evolution, Molecular ; *Gene Expression Regulation ; Genome ; Genome, Human ; Humans ; Protein Biosynthesis ; RNA Processing, Post-Transcriptional ; RNA, Untranslated/*genetics/metabolism ; Transcription, Genetic
    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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  • 10
    Publication Date: 2008-04-26
    Description: Viruses employ many different strategies to enter host cells. Vaccinia virus, a prototype poxvirus, enters cells in a pH-dependent fashion. Live cell imaging showed that fluorescent virus particles associated with and moved along filopodia to the cell body, where they were internalized after inducing the extrusion of large transient membrane blebs. p21-activated kinase 1 (PAK1) was activated by the virus, and the endocytic process had the general characteristics of macropinocytosis. The induction of blebs, the endocytic event, and infection were all critically dependent on the presence of exposed phosphatidylserine in the viral membrane, which suggests that vaccinia virus uses apoptotic mimicry to enter cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mercer, Jason -- Helenius, Ari -- New York, N.Y. -- Science. 2008 Apr 25;320(5875):531-5. doi: 10.1126/science.1155164.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉ETH Zurich, Institute of Biochemistry, Schafmattstrasse 18, ETH Honggerberg HPM E6.3 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18436786" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; *Apoptosis ; Cell Membrane/*metabolism/ultrastructure ; Humans ; Phosphatidylserines/*metabolism ; *Pinocytosis ; RNA Interference ; Vaccinia virus/*physiology ; *Virus Internalization ; p21-Activated Kinases/genetics/metabolism ; rac1 GTP-Binding Protein/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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