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  • 1
    Publication Date: 1999-05-21
    Description: Bile acids are essential for the solubilization and transport of dietary lipids and are the major products of cholesterol catabolism. Results presented here show that bile acids are physiological ligands for the farnesoid X receptor (FXR), an orphan nuclear receptor. When bound to bile acids, FXR repressed transcription of the gene encoding cholesterol 7alpha-hydroxylase, which is the rate-limiting enzyme in bile acid synthesis, and activated the gene encoding intestinal bile acid-binding protein, which is a candidate bile acid transporter. These results demonstrate a mechanism by which bile acids transcriptionally regulate their biosynthesis and enterohepatic transport.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Makishima, M -- Okamoto, A Y -- Repa, J J -- Tu, H -- Learned, R M -- Luk, A -- Hull, M V -- Lustig, K D -- Mangelsdorf, D J -- Shan, B -- New York, N.Y. -- Science. 1999 May 21;284(5418):1362-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Pharmacology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75235-9050, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10334992" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bile Acids and Salts/biosynthesis/*metabolism ; Biological Transport ; Carrier Proteins/*genetics/metabolism ; Cell Line ; Chenodeoxycholic Acid/*metabolism ; Cholesterol/metabolism ; Cholesterol 7-alpha-Hydroxylase/*genetics ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Gene Expression Regulation ; Histone Acetyltransferases ; Homeostasis ; Humans ; *Hydroxysteroid Dehydrogenases ; Ligands ; Liver/metabolism ; *Membrane Glycoproteins ; Mice ; Nuclear Receptor Coactivator 1 ; *Organic Anion Transporters, Sodium-Dependent ; Receptors, Cytoplasmic and Nuclear/chemistry/genetics/*metabolism ; *Symporters ; Transcription Factors/chemistry/genetics/*metabolism ; Transfection ; Tumor Cells, Cultured
    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: 1990-03-16
    Description: Major epidemic outbreaks of viral hepatitis in underdeveloped countries result from a type of non-A, non-B hepatitis distinct from the parenterally transmitted form. The viral agent responsible for this form of epidemic, or enterically transmitted non-A, non-B hepatitis (ET-NANBH), has been serially transmitted in cynomolgus macaques (cynos) and has resulted in typical elevation in liver enzymes and the detection of characteristic virus-like particles (VLPs) in both feces and bile. Infectious bile was used for the construction of recombinant complementary DNA libraries. One clone, ET1.1, was exogenous to uninfected human and cyno genomic liver DNA, as well as to genomic DNA from infected cyno liver. ET1.1 did however, hybridize to an approximately 7.6-kilobase RNA species present only in infected cyno liver. The translated nucleic acid sequence of a portion of ET1.1 had a consensus amino acid motif consistent with an RNA-directed RNA polymerase; this enzyme is present in all positive strand RNA viruses. Furthermore, ET1.1 specifically identified similar sequences in complementary DNA prepared from infected human fecal samples collected from five geographically distinct ET-NANBH outbreaks. Therefore, ET1.1 represents a portion of the genome of the principal viral agent, to be named hepatitis E virus, which is responsible for epidemic outbreaks of ET-NANBH.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reyes, G R -- Purdy, M A -- Kim, J P -- Luk, K C -- Young, L M -- Fry, K E -- Bradley, D W -- New York, N.Y. -- Science. 1990 Mar 16;247(4948):1335-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Virology Department, Genelabs Incorporated, Redwood City, CA 94063.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2107574" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Base Sequence ; Cloning, Molecular ; DNA/genetics ; Hepatitis E/*microbiology ; Hepatitis Viruses/*genetics ; Hepatitis, Viral, Human/*microbiology ; Humans ; Macaca fascicularis ; Molecular Sequence Data ; Polymerase Chain Reaction ; RNA Viruses/genetics ; RNA, Viral/genetics ; Restriction Mapping
    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: 2011-06-02
    Description: Members of the gammaretroviruses--such as murine leukemia viruses (MLVs), most notably XMRV [xenotropic murine leukemia virus (X-MLV)-related virus--have been reported to be present in the blood of patients with chronic fatigue syndrome (CFS). We evaluated blood samples from 61 patients with CFS from a single clinical practice, 43 of whom had previously been identified as XMRV-positive. Our analysis included polymerase chain reaction and reverse transcription polymerase chain reaction procedures for detection of viral nucleic acids and assays for detection of infectious virus and virus-specific antibodies. We found no evidence of XMRV or other MLVs in these blood samples. In addition, we found that these gammaretroviruses were strongly (X-MLV) or partially (XMRV) susceptible to inactivation by sera from CFS patients and healthy controls, which suggested that establishment of a successful MLV infection in humans would be unlikely. Consistent with previous reports, we detected MLV sequences in commercial laboratory reagents. Our results indicate that previous evidence linking XMRV and MLVs to CFS is likely attributable to laboratory contamination.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Knox, Konstance -- Carrigan, Donald -- Simmons, Graham -- Teque, Fernando -- Zhou, Yanchen -- Hackett, John Jr -- Qiu, Xiaoxing -- Luk, Ka-Cheung -- Schochetman, Gerald -- Knox, Allyn -- Kogelnik, Andreas M -- Levy, Jay A -- New York, N.Y. -- Science. 2011 Jul 1;333(6038):94-7. doi: 10.1126/science.1204963. Epub 2011 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wisconsin Viral Research Group, Milwaukee, WI 53226, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21628393" target="_blank"〉PubMed〈/a〉
    Keywords: Adolescent ; Adult ; Aged ; Antibodies, Viral/blood ; Base Sequence ; Blood/*virology ; Child ; Child, Preschool ; Complement System Proteins/immunology ; DNA Contamination ; DNA, Viral/blood ; Drug Contamination ; Fatigue Syndrome, Chronic/blood/immunology/*virology ; Female ; Humans ; Indicators and Reagents ; Leukemia Virus, Murine/genetics/isolation & purification ; Leukocytes, Mononuclear/*virology ; Male ; Middle Aged ; Molecular Sequence Data ; Polymerase Chain Reaction ; Retroviridae Infections/diagnosis/*virology ; Xenotropic murine leukemia virus-related virus/genetics/immunology/*isolation & ; purification ; Young Adult
    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: 2015-09-17
    Description: Development of functional nanoparticles can be encumbered by unanticipated material properties and biological events, which can affect nanoparticle effectiveness in complex, physiologically relevant systems. Despite the advances in bottom-up nanoengineering and surface chemistry, reductionist functionalization approaches remain inadequate in replicating the complex interfaces present in nature and cannot avoid exposure of foreign materials. Here we report on the preparation of polymeric nanoparticles enclosed in the plasma membrane of human platelets, which are a unique population of cellular fragments that adhere to a variety of disease-relevant substrates. The resulting nanoparticles possess a right-side-out unilamellar membrane coating functionalized with immunomodulatory and adhesion antigens associated with platelets. Compared to uncoated particles, the platelet membrane-cloaked nanoparticles have reduced cellular uptake by macrophage-like cells and lack particle-induced complement activation in autologous human plasma. The cloaked nanoparticles also display platelet-mimicking properties such as selective adhesion to damaged human and rodent vasculatures as well as enhanced binding to platelet-adhering pathogens. In an experimental rat model of coronary restenosis and a mouse model of systemic bacterial infection, docetaxel and vancomycin, respectively, show enhanced therapeutic efficacy when delivered by the platelet-mimetic nanoparticles. The multifaceted biointerfacing enabled by the platelet membrane cloaking method provides a new approach in developing functional nanoparticles for disease-targeted delivery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hu, Che-Ming J -- Fang, Ronnie H -- Wang, Kuei-Chun -- Luk, Brian T -- Thamphiwatana, Soracha -- Dehaini, Diana -- Nguyen, Phu -- Angsantikul, Pavimol -- Wen, Cindy H -- Kroll, Ashley V -- Carpenter, Cody -- Ramesh, Manikantan -- Qu, Vivian -- Patel, Sherrina H -- Zhu, Jie -- Shi, William -- Hofman, Florence M -- Chen, Thomas C -- Gao, Weiwei -- Zhang, Kang -- Chien, Shu -- Zhang, Liangfang -- R01DK095168/DK/NIDDK NIH HHS/ -- R01EY25090/EY/NEI NIH HHS/ -- R01HL108735/HL/NHLBI NIH HHS/ -- R25CA153915/CA/NCI NIH HHS/ -- England -- Nature. 2015 Oct 1;526(7571):118-21. doi: 10.1038/nature15373. Epub 2015 Sep 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of NanoEngineering, University of California, San Diego, La Jolla, California 92093, USA. ; Moores Cancer Center, University of California, San Diego, La Jolla, California 92093, USA. ; Department of Bioengineering, University of California, San Diego, La Jolla, California 92093, USA. ; Institute of Engineering in Medicine, University of California, San Diego, La Jolla, California 92093, USA. ; Shiley Eye Institute, University of California, San Diego, La Jolla, California 92093, USA. ; Department of Pathology, Keck School of Medicine, University of Southern California, Los Angeles, California 90033, USA. ; Veterans Administration Healthcare System, San Diego, California 92093, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26374997" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/*administration & dosage/pharmacokinetics ; Blood Platelets/*cytology ; Blood Vessels/cytology/metabolism/pathology ; Cell Membrane/*metabolism ; Collagen/chemistry/immunology ; Complement Activation/immunology ; Coronary Restenosis/blood/drug therapy/metabolism ; Disease Models, Animal ; Drug Delivery Systems/*methods ; Humans ; Macrophages/immunology ; Male ; Mice ; Nanoparticles/*administration & dosage/*chemistry ; *Platelet Adhesiveness ; Polymers/chemistry ; Rats ; Rats, Sprague-Dawley ; Staphylococcal Infections/blood/drug therapy/metabolism/microbiology ; Staphylococcus aureus/cytology/metabolism ; Taxoids/administration & dosage/pharmacokinetics ; Unilamellar Liposomes/chemistry ; Vancomycin/administration & dosage/pharmacokinetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 1993-03-19
    Description: Quantitative competitive polymerase chain reaction (QC-PCR) methods were used to quantify virion-associated human immunodeficiency virus type-1 (HIV-1) RNA in plasma from 66 patients with Centers for Disease Control stage I to IVC1 infection. HIV-1 RNA, ranging from 100 to nearly 22,000,000 copies per milliliter of plasma (corresponding to 50 to 11,000,000 virions per milliliter), was readily quantified in all subjects, was significantly associated with disease stage and CD4+ T cell counts, and decreased by as much as 235-fold with resolution of primary infection or institution of antiretroviral therapy. Plasma virus levels determined by QC-PCR correlated with, but exceeded by an average of 60,000-fold, virus titers measured by endpoint dilution culture. Quantitation of HIV-1 in plasma by QC-PCR may be useful in assessing the efficacy of antiretroviral agents, especially in early stage disease when conventional viral markers are often negative.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Piatak, M Jr -- Saag, M S -- Yang, L C -- Clark, S J -- Kappes, J C -- Luk, K C -- Hahn, B H -- Shaw, G M -- Lifson, J D -- AI25922/AI/NIAID NIH HHS/ -- AI27290/AI/NIAID NIH HHS/ -- AI32775/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1993 Mar 19;259(5102):1749-54.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of HIV and Exploratory Research, Genelabs Technologies Inc., Redwood City, CA 94063.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8096089" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/blood/drug therapy/*microbiology ; CD4-Positive T-Lymphocytes/pathology ; HIV-1/genetics/*isolation & purification/physiology ; Humans ; Leukocyte Count ; *Polymerase Chain Reaction ; RNA, Viral/*blood ; Ultracentrifugation ; Virus Replication ; Zidovudine/therapeutic use
    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: 2012-11-20
    Description: Parkinson's disease is characterized by abundant alpha-synuclein (alpha-Syn) neuronal inclusions, known as Lewy bodies and Lewy neurites, and the massive loss of midbrain dopamine neurons. However, a cause-and-effect relationship between Lewy inclusion formation and neurodegeneration remains unclear. Here, we found that in wild-type nontransgenic mice, a single intrastriatal inoculation of synthetic alpha-Syn fibrils led to the cell-to-cell transmission of pathologic alpha-Syn and Parkinson's-like Lewy pathology in anatomically interconnected regions. Lewy pathology accumulation resulted in progressive loss of dopamine neurons in the substantia nigra pars compacta, but not in the adjacent ventral tegmental area, and was accompanied by reduced dopamine levels culminating in motor deficits. This recapitulation of a neurodegenerative cascade thus establishes a mechanistic link between transmission of pathologic alpha-Syn and the cardinal features of Parkinson's disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3552321/" 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/PMC3552321/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luk, Kelvin C -- Kehm, Victoria -- Carroll, Jenna -- Zhang, Bin -- O'Brien, Patrick -- Trojanowski, John Q -- Lee, Virginia M-Y -- NS053488/NS/NINDS NIH HHS/ -- P50 NS053488/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Nov 16;338(6109):949-53. doi: 10.1126/science.1227157.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Laboratory Medicine, Institute on Aging and Center for Neurodegenerative Disease Research, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104-4283, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23161999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Corpus Striatum/drug effects/*metabolism/pathology ; Dopamine ; Dopaminergic Neurons/drug effects/metabolism/pathology ; Injections ; Lewy Bodies/drug effects/*metabolism/pathology ; Mice ; Parkinsonian Disorders/*metabolism/pathology ; Protein Folding ; Protein Transport ; Recombinant Proteins/administration & dosage/chemistry/metabolism ; Substantia Nigra/drug effects/metabolism/pathology ; alpha-Synuclein/administration & dosage/chemistry/*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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  • 7
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-09-02
    Description: Electrophoretic analysis of glucose-6-phosphate dehydrogenase was performed on polyp tissue from three black female patients with Gardner syndrome and who are heterozygous for the A and B forms of this enzyme. Polyp tissues from the three patients displayed the AB phenotype. This finding suggests a multiclonal origin of polyps in Gardner syndrome. Studies of tumors originating from such polyps may provide information about the sequence of cellular events leading to malignant transformation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsu, S H -- Luk, G D -- Krush, A J -- Hamilton, S R -- Hoover, H H Jr -- 1 R01AI17431-01A1/AI/NIAID NIH HHS/ -- R01 AM 20656-04/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 2;221(4614):951-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879192" target="_blank"〉PubMed〈/a〉
    Keywords: Clone Cells/pathology ; Female ; Gardner Syndrome/enzymology/*genetics/pathology ; Glucosephosphate Dehydrogenase/genetics ; Humans ; Isoenzymes/genetics ; Polyps/enzymology/*genetics ; X Chromosome
    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: 1982-04-02
    Description: The ornithine decarboxylase inhibitor DL-alpha-difluoromethyl ornithine inhibited a proliferation-associated increase in ornithine decarboxylase activity in cultured human promyelocytic leukemia cells, resulting in a marked suppression of cell proliferation and subsequent cell loss. It also inhibited increases in ornithine decarboxylase activity associated with the phorbol ester-induced conversion of promyelocytic HL-60 cells to monocyte-like cells and the retinoic acid-induced conversion to granulocyte-like cells. However, the inhibition of ornithine decarboxylase activity did not prevent cellular differentiation. These results suggest that polyamine biosynthesis has a specific role in cell proliferation rather than in inducing differentiation that is not accompanied by proliferation. The data also demonstrate that cessation of proliferation in HL-60 cells is not necessarily associated with differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Luk, G D -- Civin, C I -- Weissman, R M -- Baylin, S B -- AM-27447/AM/NIADDK NIH HHS/ -- CA-18404/CA/NCI NIH HHS/ -- HL-19157/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1982 Apr 2;216(4541):75-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6950518" target="_blank"〉PubMed〈/a〉
    Keywords: Carboxy-Lyases/*physiology ; Cell Adhesion ; Cell Differentiation ; Cell Division ; Cells, Cultured ; Female ; Granulocytes/pathology ; Humans ; Leukemia, Myeloid, Acute/*enzymology/pathology ; Macrophages/pathology ; Ornithine Decarboxylase/*physiology ; Polyamines/biosynthesis ; Tetradecanoylphorbol Acetate/pharmacology ; Tretinoin/pharmacology
    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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