ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

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
  • Male  (4)
  • American Association for the Advancement of Science (AAAS)  (4)
  • Wiley
  • 2010-2014  (4)
Collection
Publisher
Years
Year
  • 1
    Publication Date: 2010-05-15
    Description: It is predicted that climate change will cause species extinctions and distributional shifts in coming decades, but data to validate these predictions are relatively scarce. Here, we compare recent and historical surveys for 48 Mexican lizard species at 200 sites. Since 1975, 12% of local populations have gone extinct. We verified physiological models of extinction risk with observed local extinctions and extended projections worldwide. Since 1975, we estimate that 4% of local populations have gone extinct worldwide, but by 2080 local extinctions are projected to reach 39% worldwide, and species extinctions may reach 20%. Global extinction projections were validated with local extinctions observed from 1975 to 2009 for regional biotas on four other continents, suggesting that lizards have already crossed a threshold for extinctions caused by climate change.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sinervo, Barry -- Mendez-de-la-Cruz, Fausto -- Miles, Donald B -- Heulin, Benoit -- Bastiaans, Elizabeth -- Villagran-Santa Cruz, Maricela -- Lara-Resendiz, Rafael -- Martinez-Mendez, Norberto -- Calderon-Espinosa, Martha Lucia -- Meza-Lazaro, Rubi Nelsi -- Gadsden, Hector -- Avila, Luciano Javier -- Morando, Mariana -- De la Riva, Ignacio J -- Victoriano Sepulveda, Pedro -- Rocha, Carlos Frederico Duarte -- Ibarguengoytia, Nora -- Aguilar Puntriano, Cesar -- Massot, Manuel -- Lepetz, Virginie -- Oksanen, Tuula A -- Chapple, David G -- Bauer, Aaron M -- Branch, William R -- Clobert, Jean -- Sites, Jack W Jr -- New York, N.Y. -- Science. 2010 May 14;328(5980):894-9. doi: 10.1126/science.1184695.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of California, Santa Cruz, CA 95064, USA. lizardrps@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20466932" target="_blank"〉PubMed〈/a〉
    Keywords: Acclimatization ; Animals ; *Biodiversity ; Biological Evolution ; Body Temperature ; *Climate Change ; *Ecosystem ; *Extinction, Biological ; Female ; Forecasting ; Geography ; Global Warming ; *Lizards/genetics/physiology ; Male ; Mexico ; Models, Biological ; Phylogeny ; Population Dynamics ; Reproduction ; Seasons ; Selection, Genetic ; Temperature
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 2011-06-02
    Description: The retrovirus XMRV (xenotropic murine leukemia virus-related virus) has been detected in human prostate tumors and in blood samples from patients with chronic fatigue syndrome, but these findings have not been replicated. We hypothesized that an understanding of when and how XMRV first arose might help explain the discrepant results. We studied human prostate cancer cell lines CWR22Rv1 and CWR-R1, which produce XMRV virtually identical to the viruses recently found in patient samples, as well as their progenitor human prostate tumor xenograft (CWR22) that had been passaged in mice. We detected XMRV infection in the two cell lines and in the later passage xenografts, but not in the early passages. In particular, we found that the host mice contained two proviruses, PreXMRV-1 and PreXMRV-2, which share 99.92% identity with XMRV over 〉3.2-kilobase stretches of their genomes. We conclude that XMRV was not present in the original CWR22 tumor but was generated by recombination of two proviruses during tumor passaging in mice. The probability that an identical recombinant was generated independently is negligible (~10(-12)); our results suggest that the association of XMRV with human disease is due to contamination of human samples with virus originating from this recombination event.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3278917/" 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/PMC3278917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paprotka, Tobias -- Delviks-Frankenberry, Krista A -- Cingoz, Oya -- Martinez, Anthony -- Kung, Hsing-Jien -- Tepper, Clifford G -- Hu, Wei-Shau -- Fivash, Matthew J Jr -- Coffin, John M -- Pathak, Vinay K -- P30 CA093373/CA/NCI NIH HHS/ -- R01CA150197/CA/NCI NIH HHS/ -- R37 CA 089441/CA/NCI NIH HHS/ -- R37 CA089441/CA/NCI NIH HHS/ -- R37 CA089441-11/CA/NCI NIH HHS/ -- ZIA BC011339-02/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):97-101. doi: 10.1126/science.1205292. Epub 2011 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Viral Mutation Section, HIV Drug Resistance Program, National Cancer Institute at Frederick, Frederick, MD 21702, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21628392" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Line, Tumor/*virology ; DNA Contamination ; DNA, Viral/analysis ; Endogenous Retroviruses/genetics ; Fatigue Syndrome, Chronic/virology ; Gammaretrovirus/*genetics ; Genes, env ; Genes, gag ; Humans ; Male ; Mice ; Mice, Nude ; Neoplasm Transplantation ; Polymerase Chain Reaction ; Prostatic Neoplasms/*virology ; Proviruses/genetics/isolation & purification ; *Recombination, Genetic ; Transplantation, Heterologous ; Xenotropic murine leukemia virus-related virus/*genetics/*isolation & ; purification
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 3
    Publication Date: 2011-08-20
    Description: Most cancer cells are characterized by aneuploidy, an abnormal number of chromosomes. We have identified a clue to the mechanistic origins of aneuploidy through integrative genomic analyses of human tumors. A diverse range of tumor types were found to harbor deletions or inactivating mutations of STAG2, a gene encoding a subunit of the cohesin complex, which regulates the separation of sister chromatids during cell division. Because STAG2 is on the X chromosome, its inactivation requires only a single mutational event. Studying a near-diploid human cell line with a stable karyotype, we found that targeted inactivation of STAG2 led to chromatid cohesion defects and aneuploidy, whereas in two aneuploid human glioblastoma cell lines, targeted correction of the endogenous mutant alleles of STAG2 led to enhanced chromosomal stability. Thus, genetic disruption of cohesin is a cause of aneuploidy in human cancer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3374335/" 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/PMC3374335/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Solomon, David A -- Kim, Taeyeon -- Diaz-Martinez, Laura A -- Fair, Joshlean -- Elkahloun, Abdel G -- Harris, Brent T -- Toretsky, Jeffrey A -- Rosenberg, Steven A -- Shukla, Neerav -- Ladanyi, Marc -- Samuels, Yardena -- James, C David -- Yu, Hongtao -- Kim, Jung-Sik -- Waldman, Todd -- CA097257/CA/NCI NIH HHS/ -- R01 CA133662/CA/NCI NIH HHS/ -- R01 CA138212/CA/NCI NIH HHS/ -- R01 CA169345/CA/NCI NIH HHS/ -- R01CA115699/CA/NCI NIH HHS/ -- R21CA143282/CA/NCI NIH HHS/ -- Z01 HG200337-01/Intramural NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2011 Aug 19;333(6045):1039-43. doi: 10.1126/science.1203619.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Oncology, Lombardi Comprehensive Cancer Center, Georgetown University School of Medicine, Washington, DC 20057, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21852505" target="_blank"〉PubMed〈/a〉
    Keywords: *Aneuploidy ; Antigens, Nuclear/*genetics/*physiology ; Cell Cycle ; Cell Line ; Cell Line, Tumor ; Chromatids/physiology ; *Chromosomal Instability ; Chromosomes, Human, X/genetics ; Female ; Gene Deletion ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Silencing ; Gene Targeting ; Glioblastoma/*genetics ; Humans ; Karyotyping ; Male ; Melanoma/genetics ; Mutation ; Neoplasms/*genetics ; Polymorphism, Single Nucleotide ; Sarcoma, Ewing/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 4
    Publication Date: 2014-05-09
    Description: Throughout life, new neurons are continuously added to the dentate gyrus. As this continuous addition remodels hippocampal circuits, computational models predict that neurogenesis leads to degradation or forgetting of established memories. Consistent with this, increasing neurogenesis after the formation of a memory was sufficient to induce forgetting in adult mice. By contrast, during infancy, when hippocampal neurogenesis levels are high and freshly generated memories tend to be rapidly forgotten (infantile amnesia), decreasing neurogenesis after memory formation mitigated forgetting. In precocial species, including guinea pigs and degus, most granule cells are generated prenatally. Consistent with reduced levels of postnatal hippocampal neurogenesis, infant guinea pigs and degus did not exhibit forgetting. However, increasing neurogenesis after memory formation induced infantile amnesia in these species.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Akers, Katherine G -- Martinez-Canabal, Alonso -- Restivo, Leonardo -- Yiu, Adelaide P -- De Cristofaro, Antonietta -- Hsiang, Hwa-Lin Liz -- Wheeler, Anne L -- Guskjolen, Axel -- Niibori, Yosuke -- Shoji, Hirotaka -- Ohira, Koji -- Richards, Blake A -- Miyakawa, Tsuyoshi -- Josselyn, Sheena A -- Frankland, Paul W -- MOP74650/Canadian Institutes of Health Research/Canada -- MOP86762/Canadian Institutes of Health Research/Canada -- New York, N.Y. -- Science. 2014 May 9;344(6184):598-602. doi: 10.1126/science.1248903.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Neurosciences and Mental Health, The Hospital for Sick Children, Toronto, M5G 1X8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24812394" target="_blank"〉PubMed〈/a〉
    Keywords: Amnesia/*pathology/*physiopathology ; Animals ; Dentate Gyrus/cytology ; Female ; Guinea Pigs ; Hippocampus/*cytology ; Male ; *Memory ; Mice ; Mice, Inbred C57BL ; *Neurogenesis ; Neurons/cytology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...