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  • 1
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    Thalamic control of visceral nociception mediated by T-type Ca2+ channels (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-10-04
    Description: Sensations from viscera, like fullness, easily become painful if the stimulus persists. Mice lacking alpha1G T-type Ca2+ channels show hyperalgesia to visceral pain. Thalamic infusion of a T-type blocker induced similar hyperalgesia in wild-type mice. In response to visceral pain, the ventroposterolateral thalamic neurons evokeda surge of single spikes, which then slowly decayed as T type-dependent burst spikes gradually increased. In alpha1G-deficient neurons, the single-spike response persisted without burst spikes. These results indicate that T-type Ca2+ channels underlie an antinociceptive mechanism operating in the thalamus andsupport the idea that burst firing plays a critical role in sensory gating in the thalamus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Daesoo -- Park, Donghyun -- Choi, Soonwook -- Lee, Sukchan -- Sun, Minjeong -- Kim, Chanki -- Shin, Hee-Sup -- New York, N.Y. -- Science. 2003 Oct 3;302(5642):117-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Creative Research Initiative Center for Calcium and Learning, Korea Institutes of Science and Technology, Seoul 136-791, Korea.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14526084" target="_blank"〉PubMed〈/a〉
    Keywords: Abdominal Pain/physiopathology ; Acetic Acid/pharmacology ; Action Potentials ; Analysis of Variance ; Animals ; Calcium Channel Blockers/pharmacology ; Calcium Channels, T-Type/genetics/*physiology ; Female ; Magnesium Sulfate/pharmacology ; Male ; Mibefradil/pharmacology ; Mice ; Mice, Inbred C57BL ; Mutation ; Neurons/physiology ; Pain/*physiopathology ; Pain Measurement ; Ventral Thalamic Nuclei/*physiology ; Viscera
    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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  • 2
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    Inactivation of TNF signaling by rationally designed dominant-negative TNF variants (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-09-27
    Description: Tumor necrosis factor (TNF) is a key regulator of inflammatory responses and has been implicated in many pathological conditions. We used structure-based design to engineer variant TNF proteins that rapidly form heterotrimers with native TNF to give complexes that neither bind to nor stimulate signaling through TNF receptors. Thus, TNF is inactivated by sequestration. Dominant-negative TNFs represent a possible approach to anti-inflammatory biotherapeutics, and experiments in animal models show that the strategy can attenuate TNF-mediated pathology. Similar rational design could be used to engineer inhibitors of additional TNF superfamily cytokines as well as other multimeric ligands.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steed, Paul M -- Tansey, Malu G -- Zalevsky, Jonathan -- Zhukovsky, Eugene A -- Desjarlais, John R -- Szymkowski, David E -- Abbott, Christina -- Carmichael, David -- Chan, Cheryl -- Cherry, Lisa -- Cheung, Peter -- Chirino, Arthur J -- Chung, Hyo H -- Doberstein, Stephen K -- Eivazi, Araz -- Filikov, Anton V -- Gao, Sarah X -- Hubert, Rene S -- Hwang, Marian -- Hyun, Linus -- Kashi, Sandhya -- Kim, Alice -- Kim, Esther -- Kung, James -- Martinez, Sabrina P -- Muchhal, Umesh S -- Nguyen, Duc-Hanh T -- O'Brien, Christopher -- O'Keefe, Donald -- Singer, Karen -- Vafa, Omid -- Vielmetter, Jost -- Yoder, Sean C -- Dahiyat, Bassil I -- New York, N.Y. -- Science. 2003 Sep 26;301(5641):1895-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Xencor, 111 West Lemon Avenue, Monrovia, CA 91016, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/14512626" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Substitution ; Animals ; Antigens, CD/metabolism ; Apoptosis ; Arthritis, Experimental/drug therapy ; Biopolymers ; Caspases/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Computer Simulation ; Disease Progression ; Enzyme-Linked Immunosorbent Assay ; Female ; Galactosamine/pharmacology ; HeLa Cells ; Humans ; Liver/drug effects ; NF-kappa B/metabolism ; Point Mutation ; *Protein Engineering ; Rats ; Receptors, Tumor Necrosis Factor/metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; *Signal Transduction ; Transcription Factor RelA ; Transcription, Genetic ; Tumor Necrosis Factor-alpha/*antagonists & ; inhibitors/genetics/metabolism/*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)
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  • 3
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    Positional cloning of the human quantitative trait locus underlying taste sensitivity to phenylthiocarbamide (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-22
    Description: The ability to taste the substance phenylthiocarbamide (PTC) has been widely used for genetic and anthropological studies, but genetic studies have produced conflicting results and demonstrated complex inheritance for this trait. We have identified a small region on chromosome 7q that shows strong linkage disequilibrium between single-nucleotide polymorphism (SNP) markers and PTC taste sensitivity in unrelated subjects. This region contains a single gene that encodes a member of the TAS2R bitter taste receptor family. We identified three coding SNPs giving rise to five haplotypes in this gene worldwide. These haplotypes completely explain the bimodal distribution of PTC taste sensitivity, thus accounting for the inheritance of the classically defined taste insensitivity and for 55 to 85% of the variance in PTC sensitivity. Distinct phenotypes were associated with specific haplotypes, which demonstrates that this gene has a direct influence on PTC taste sensitivity and that sequence variants at different sites interact with each other within the encoded gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, Un-kyung -- Jorgenson, Eric -- Coon, Hilary -- Leppert, Mark -- Risch, Neil -- Drayna, Dennis -- M01-RR00064/RR/NCRR NIH HHS/ -- T32 HG00044/HG/NHGRI NIH HHS/ -- Z01-000046-04/PHS HHS/ -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1221-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉National Institute on Deafness and Other Communication Disorders, National Institutes of Health, 5 Research Court, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595690" target="_blank"〉PubMed〈/a〉
    Keywords: Alleles ; Amino Acid Substitution ; Animals ; Cebidae/genetics ; Chromosomes, Human, Pair 7/genetics ; Cloning, Molecular ; Computational Biology ; Continental Population Groups/genetics ; Evolution, Molecular ; Female ; Genetic Linkage ; Haplotypes ; Heterozygote ; Hominidae/genetics ; Homozygote ; Humans ; Linkage Disequilibrium ; Macaca fascicularis/genetics ; Male ; *Phenylthiourea ; *Polymorphism, Single Nucleotide ; *Quantitative Trait Loci ; Receptors, Cell Surface/chemistry/*genetics/physiology ; Receptors, G-Protein-Coupled ; Sequence Analysis, DNA ; Taste/*genetics ; Taste Threshold
    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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    Development. What makes an embryo stick? (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-01-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fazleabas, Asgerally T -- Kim, J Julie -- New York, N.Y. -- Science. 2003 Jan 17;299(5605):355-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Obstetrics and Gynecology, University of Illinois, Chicago, IL 60612, USA. asgi@uic.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12532005" target="_blank"〉PubMed〈/a〉
    Keywords: Blastocyst/physiology ; Cell Adhesion ; Cell Adhesion Molecules/metabolism ; Cells, Cultured ; Coculture Techniques ; *Embryo Implantation ; Endometrium/cytology/*physiology ; Epithelial Cells/physiology ; Female ; Humans ; L-Selectin/*metabolism ; Ligands ; Oligosaccharides/metabolism ; Pregnancy ; Signal Transduction ; Trophoblasts/*metabolism ; Up-Regulation
    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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