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  • American Society of Hematology  (6)
  • Geological Society of London  (5)
  • American Association for the Advancement of Science (AAAS)  (1)
  • American Institute of Physics (AIP)
  • Amsterdam : Elsevier
  • 2005-2009  (12)
  • 2000-2004
  • 1990-1994
  • 1985-1989
  • 2005  (12)
Collection
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  • 2005-2009  (12)
  • 2000-2004
  • 1990-1994
  • 1985-1989
Year
  • 1
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    Transmission of equine influenza virus to dogs (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-09-28
    Description: Molecular and antigenic analyses of three influenza viruses isolated from outbreaks of severe respiratory disease in racing greyhounds revealed that they are closely related to H3N8 equine influenza virus. Phylogenetic analysis indicated that the canine influenza virus genomes form a monophyletic group, consistent with a single interspecies virus transfer. Molecular changes in the hemagglutinin suggested adaptive evolution in the new host. The etiologic role of this virus in respiratory disease was supported by the temporal association of rising antibody titers with disease and by experimental inoculation studies. The geographic expansion of the infection and its persistence for several years indicate efficient transmission of canine influenza virus among greyhounds. Evidence of infection in pet dogs suggests that this infection may also become enzootic in this population.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crawford, P C -- Dubovi, Edward J -- Castleman, William L -- Stephenson, Iain -- Gibbs, E P J -- Chen, Limei -- Smith, Catherine -- Hill, Richard C -- Ferro, Pamela -- Pompey, Justine -- Bright, Rick A -- Medina, Marie-Jo -- Johnson, Calvin M -- Olsen, Christopher W -- Cox, Nancy J -- Klimov, Alexander I -- Katz, Jacqueline M -- Donis, Ruben O -- New York, N.Y. -- Science. 2005 Oct 21;310(5747):482-5. Epub 2005 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉College of Veterinary Medicine, University of Florida, Gainesville, FL 32611, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16186182" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Antibodies, Viral/blood ; Cell Line ; Cytopathogenic Effect, Viral ; Disease Outbreaks/*veterinary ; Dog Diseases/epidemiology/pathology/*transmission/*virology ; Dogs ; Florida/epidemiology ; Hemagglutinin Glycoproteins, Influenza Virus/chemistry/genetics ; Horse Diseases/transmission/*virology ; Horses ; *Influenza A Virus, H3N8 Subtype/classification/immunology/isolation & ; purification/pathogenicity ; Molecular Sequence Data ; Orthomyxoviridae Infections/epidemiology/transmission/*veterinary/virology ; Phylogeny ; Respiratory System/pathology ; Sequence Analysis, RNA ; Species Specificity ; United States/epidemiology ; Virus Shedding
    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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    BLIMP-1 Is a Target of Cellular Stress and Downstream of the Unfolded Protein Response. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: Human B lymphocyte-induced maturation protein-1 (BLIMP-1) was originally described as a repressor of the interferon-beta response to viral infection. Subsequently, the murine orthologue was identified as a regulator of plasma cell differentiation. The involvement of BLIMP-1 in hemopoietic differentiation is not restricted to the B-cell lineage as BLIMP-1 is induced during differentiation of myeloid progenitors. During in vitro macrophage and plasma cell differentiation the expression of BLIMP-1 is cytokine driven. However, the BLIMP-1 response to virus infection can be reproduced by transfection with double-stranded RNA (dsRNA), indicating that BLIMP-1 is a target of dsRNA responsive signaling pathways. A central regulator of the intracellular response to viral infection is the interferon-inducible double-stranded RNA activated kinase, PKR. PKR belongs to a family of kinases that phosphorylate the eukaryotic translation initiation factor 2-alpha (eIF2α) and activate common downstream signaling pathways. PERK, the endoplasmic reticulum (ER) PKR-homologue is activated during the unfolded protein response (UPR), a stress response involved in both macrophage activation and terminal B-cell differentiation. This suggested the hypothesis that BLIMP-1 may represent a shared target of signaling pathways in the response to cellular stresses such as virus infection and the UPR. In this study we demonstrate that BLIMP-1 is rapidly upregulated during the UPR in human myeloid and B-cell lines. This response is conserved in primary murine macrophages, in which mimics of physiological stress and classical activation stimuli also induce Blimp-1. During the UPR, BLIMP-1 mRNA is induced at the level of transcription, with enhanced recruitment of RNA polymerase II to the BLIMP-1 promoter. Furthermore the stress response is limited to induction of BLIMP-1α mRNA and does not affect levels of an alternate transcript encoding a truncated protein, BLIMP-1β. The common induction of BLIMP-1 mRNA by stimuli which trigger the UPR supports the hypothesis that BLIMP-1 is a target of the eIF2α kinase family. To test this hypothesis directly, we employed a dominant negative mutant PERK. Our data demonstrate that the BLIMP-1 response to UPR stress is dependent on an intact PERK signaling pathway. Collectively our results provide evidence for a novel link between cellular stress, the eIF2α kinase family and a regulator of differentiation in macrophages and B-cells.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 3
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    Global Haemostasis in Critically Ill Patients with Sepsis: Evidence for a Prothrombotic State. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: Activation of haemostasis in sepsis may lead to microvascular thrombosis and progression to multiorgan failure (MOF). Almost all critically ill patients with sepsis have abnormal coagulation screens but these are unlikely to adequately represent the state of a patient’s haemostatic system and global assays may be more useful. Normal controls (n=32) and critically ill patients with sepsis (n=39) were recruited. Coagulation factors, antithrombin (AT) and protein C (PC) were measured. Thrombin generation was measured using the calibrated automated thrombogram (CAT) in platelet rich (PRP) and poor (PPP) plasma. Low dose tissue factor (6pM) activated whole blood Rotem® was measured and the first derivative of the trace gave a velocity of clot firmness. Haemostatic changes in sepsis compared to normal controls Controls Controls mean (SD) Sepsis mean (SD) P Apparent effect of change PT (s) 11.7 (0.5) 19.7 (5.9) 0.001 Anticoagulant aPTT (s) 27 (3.4) 44.1 (18.2) 0.001 Anticoagulant Fibrinogen g/l 2.8 (0.57) 5.3 (2.1) 0.001 Prothrombotic FII IU/dl 100 (12.1) 64 (32.2) 0.001 Anticoagulant FV IU/dl 116 (22.9) 96 (55.2) 0.03 Anticoagulant FVII IU/dl 130 (31.1) 58 (33.5) 0.001 Anticoagulant FVIII IU/dl 107 (31.5) 242 (96) 0.001 Prothrombotic FIX IU/dl 101 (16.5) 112 (51.3) NS Neutral FX IU/dl 123 (16.6) 75 (42.1) 0.001 Anticoagulant FXI IU/dl 116 (15.7) 80 (41) 0.001 Anticoagulant FXII IU/dl 125 (27.8) 56 (29.4) 0.001 Neutral PC % 127 (20) 66 (37) 0.001 Prothrombotic AT IU/dl 103 (8) 64 (29) 0.001 Prothrombotic CAT in PRP Lag time (min) 17 (8) 30 (23) 0.02 Delayed ETP (nM.min) 1395 (488) 1270 (573) NS Neutral Peak thrombin (nM) 76 (40) 55 (31) 0.02 Anticoagulant Time to peak (min) 32 (12) 50 (29) 0.001 Delayed CAT in PPP Lag time (min) 2.4 (0.9) 5.1 (5.4) 0.001 Delayed ETP (nM.min) 1681 (281) 1645 (442) NS Neutral Peak thrombin (nM) 454 (100) 343 (146) 0.001 Anticoagulant Time to peak (min) 4.2 (1.2) 6.8 (6.6) 0.001 Delayed Low dose tissue factor Rotem Clot time (s) 818 (271) 1170 (766) 0.04 Delayed Alpha angle (°) 51 (12) 67 (17) 0.005 Prothrombotic MCF (mm) 51 (12) 67 (17) 0.001 Prothrombotic Max vel (mm/s) 6.5 (3.0) 10.9 (7.4) 0.005 Prothrombotic Time to Vmax (s) 1040 (334) 1079 (650) NS Neutral AUC 51 (12) 62 (24) 0.001 Prothrombotic The results show that despite decreased levels of factors II, V, VII, XI and XII (correlation with decreased albumin, P
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 4
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    MHC Class-II Expression Reveals Differential Regulation of BLIMP-1 Target Genes. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: BLIMP-1 initiates plasma cell differentiation by inhibiting the expression of a limited set of transcription factor genes. BLIMP-1 mediates repression of its targets by promoter occupancy and recruitment of the Groucho corepressor, histone deacetylase and the G9a lysine methyltransferase. The relative contribution of these mechanisms to the stable silencing of BLIMP-1 target genes in plasma cells is not known. Epigenetic changes initiated by BLIMP-1 could be maintained by independent factors or alternatively may be dependent on continuous occupancy of the promoter by BLIMP-1. The aim of this study was to investigate the mechanisms operating at two well-defined BLIMP-1 target genes, MHC2TA and PAX-5. Repression of PAX-5 is essential for extinction of the B-cell phenotype, while repression of MHC2TA mediates the loss of MHC class-II expression characteristic of plasma cell differentiation. PAX-5 is silenced in virtually all cases of myeloma, whereas MHC class-II continues to be expressed in a subset of primary myeloma cells and many myeloma cell lines. Using chromatin immunoprecipitation we demonstrate that BLIMP-1 constitutively binds MHC2TA promoter-3 and is present equally in MHC2TA expressing and non-expressing myeloma cell lines. In expressing cells MHC2TA promoter-3 is associated with acetylation of histone H3 lysine-9, a marker of open chromatin, whereas histone H3 lysine-9 is neither acetylated nor methylated in non-expressing cells. In contrast the PAX-5 promoter is associated with trimethylation of histone H3 lysine-9, a marker of repressed heterochromatin, in all the cell lines examined, but constitutive BLIMP-1 occupancy is not detectable. Although BLIMP-1 does not silence MHC2TA expression in the MHC class-II positive U266 cell line, it is mediating transcriptional repression, since siRNA knockdown of BLIMP-1 is associated with elevated MHC2TA mRNA and MHC class-II surface expression. In contrast PAX-5 mRNA and its target CD19 continue to be repressed. MHC class-II re-expression was associated with loss of CD138 and the entry of the majority of cells into apoptosis. Our data demonstrate that MHC class-II expression in myeloma cell lines is associated with defective silencing of MHC2TA despite BLIMP-1 occupancy, and reveal differences in the contribution of epigenetic modifications and promoter occupancy in the maintenance of target gene silencing by BLIMP-1. Loss of BLIMP-1 results in a partial reversion of plasma cell phenotype that is associated with induction of apoptosis. As continual high levels of BLIMP-1 expression appear to be critical for plasma cell survival, suppression of BLIMP-1 represents a potential therapeutic pathway.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology
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  • 5
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    Functional abnormalities of heparan sulfate in mucopolysaccharidosis-I are associated with defective biologic activity of FGF-2 on human multipotent progenitor cells (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-09-15
    Description: In mucopolysaccharidosis-I (MPS-I), α-L-iduronidase deficiency leads to progressive heparan sulfate (HS) and dermatan sulfate (DS) glycosaminoglycan (GAG) accumulation. The functional consequences of these accumulated molecules are unknown. HS critically influences tissue morphogenesis by binding to and modulating the activity of several cytokines (eg, fibroblast growth factors [FGFs]) involved in developmental patterning. We recently isolated a multipotent progenitor cell from postnatal human bone marrow, which differentiates into cells of all 3 embryonic lineages. The availability of multipotent progenitor cells from healthy volunteers and patients with MPS-I (Hurler syndrome) provides a unique opportunity to directly examine the functional effects of abnormal HS on cytokine-mediated stem-cell proliferation and survival. We demonstrate here that abnormally sulfated HS in Hurler multipotent progenitor cells perturb critical FGF-2–FGFR1-HS interactions, resulting in defective FGF-2–induced proliferation and survival of Hurler multipotent progenitor cells. Both the mitogenic and survival-promoting activities of FGF-2 were restored by substitution of Hurler HS by normal HS. This perturbation of critical HS–cytokine receptor interactions may represent a mechanism by which accumulated HS contributes to the developmental pathophysiology of Hurler syndrome. Similar mechanisms may operate in the pathogenesis of other diseases where structurally abnormal GAGs accumulate.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 6
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    Selective Modulation of the BMP Signaling Pathway Has Distinct Effects on Long-Term In Vitro Maintenance of Primitive Hematopoietic Progenitors in Human Umbilical Cord Blood. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: Factors responsible for long-term survival and proliferation of human hematopoietic stem cells (hHSC), and their mechanisms of action, remain to be defined. We previously showed that specific O-sulfated heparan sulfate (OS-HS) improves human long-term culture initiating cell (LTC-IC) maintenance for up to 5 wks in vitro. This is related to the ability of OS-HS to bind to and modulate the activity of heparin-binding cytokines on primitive hematopoietic progenitors (PHP). Recent studies indicate that bone morphogenetic proteins (BMPs) influence the development of embryonic hematopoiesis and also augment short-term survival and proliferation of hHSC. Since HS may modulate BMP activity, we examined how combinations of OS-HS, BMPs and specific BMP antagonists influence PHP in umbilical cord blood (UCB). First, we confirmed by real-time quantitative RT-PCR (qRT-PCR) that UCB CD34+ and/or CD34+/CD38− cells (using linear mRNA amplification) constitutively express transcripts for BMP-4 and its inhibitor Chordin, BMP receptors BMPR-IA, BMPR-IB, BMPR-II, AcvR-II and AcvR-IIB, downstream signaling proteins SMAD-1 and -5, and target genes upregulated by BMPs including Inhibitors of DNA binding (Id) proteins 1–4, and determined their relative levels of expression. BMP-4 upregulated Id2 expression 17-fold, confirming that the BMP signaling pathway is functionally active in CD34+ cells. Next, we demonstrated that OS-HS may protect BMP-4 from its inhibitors, using Western immunoblotting of immunoprecipitated proteins to show that direct binding of the antagonist Chordin to BMP-4 is inhibited by OS-HS in a dose-dependent manner. Finally, we examined the effect of exogenous supplementation with 6 BMPs, or inhibition of endogenous BMPs by 7 antagonists, on short-term (2 wk) and long-term (5 wk) LTC-IC maintenance in UCB CD34+/CD38− cells cultured in presence of OS-HS, Flt3-ligand and thrombopoietin. Long-term LTC-IC maintenance was enhanced by BMP-4 (LTC-IC maintenance: 164 +/− 11% compared to culture without BMP-4; P=0.0001) but reduced by BMP-2 or BMP-7 (P
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    Electronic ISSN: 1528-0020
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  • 7
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    μ Opioid Receptor Stimulates a Growth Promoting and Pro-Angiogenic Tumor Microenvironment by Transactivating VEGF Receptor-2/Flk-1. (2005)
    American Society of Hematology
    Details
    Publication Date: 2005-11-16
    Description: Like VEGF, morphine stimulates MAPK/ERK and Akt, leading to the promotion of angiogenesis via NO dependent signaling (Cancer Res62: 4491, 2002). Morphine acts via pertussis toxin (PT)-dependent G-protein coupled receptors (GPCRS), while VEGF acts via receptor tyrosine kinases (RTKs). We showed that PT-dependent GPCRs transactivate VEGF receptor-2/Flk1 via small GTPase RhoA (JBC277: 4679, 2002; JBC278:20738, 2003). Therefore, we hypothesized that morphine via the mu opioid receptor (MOR) transactivates Flk1 and promotes a pro-angiogenic microenvironment. Morphine-induced proliferation of human umbilical vein endothelial cells (HUVEC) was completely abrogated by Y-27632 (100 μM), a highly selective and potent inhibitor of Rho-associated protein kinases, suggesting the activation of Rho signaling by morphine. Addition of 1 μM morphine potentiated VEGF-induced (10 ng/ml) proliferation of HUVEC by 25%. We observed a 30% increase in intracellular calcium release after VEGF stimulation of HUVEC pre-incubated with morphine as compared to HUVEC pre-incubated with PBS, detected by a change in the fluorescence ratio of the Fura-2 AM dye. These findings show that morphine, via MOR and Rho signaling, transactivates Flk1 leading to the stimulation of calcium signaling and endothelial cell proliferation. To functionally corroborate our hypothesis, we used MOR knockout (MOR-KO) mice and injected them with MOR-replete T241 fibrosarcoma cells. T241 fibrosarcoma tumor growth in vivo showed appearance of palpable and measurable tumors 2 days earlier in wild type (wt) as compared to MOR-KO mice. Tumor growth and angiogenesis were decreased by 20–35% in MOR-KO mice as compared to wt littermates during 3 weeks of tumor growth. None of the MOR-KO showed signs of lung metastasis versus 40% wt mice with metastasis. Morphine (1.42 for the first 2 wks and 2.14 mg/Kg/day later, respectively) stimulated 20–35% tumor growth in wt, but not in MOR-KO mice. Western immunoblotting showed a 10-fold increase in the expression of phospho-Flk1 in morphine treated wt tumors as compared to PBS-treated wt mice. Morphine did not stimulate phospho-Flk1 expression in MOR-KO mice. Western analysis of immunoprecipitates obtained with α-MOR antibody showed the expression of Flk1 and phospho-Flk1 in wt, but were not expressed in MOR-KO tumors. Thus, MOR stimulates the transactivation of Flk1 in wt mice but not in MOR-KO. These in vitro and in vivo data using MOR-KO mice and the MOR agonist, morphine, show that MOR stimulates endothelial proliferation, angiogenesis and promotes tumor growth and metastasis directly as well as by transactivating Flk1 phosphorylation. We speculate that MOR is a critical component of the ‘angiogenic switch’, which regulates the pro-angiogenic and growth promoting tumor microenvironment. Thus, MOR provides a novel target for developing anti-angiogenic therapies.
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
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  • 8
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    Basic and ultrabasic volcanic rocks from the Argyll Group (Dalradian) of NE Scotland (2005)
    Geological Society of London
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    Publication Date: 2005-11-01
    Print ISSN: 0036-9276
    Electronic ISSN: 2041-4951
    Topics: Geosciences
    Published by Geological Society of London
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  • 9
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    Investigating the record of Permian climate change from argillaceous sedimentary rocks, Oman (2005)
    Geological Society of London
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    Publication Date: 2005-07-01
    Print ISSN: 0016-7649
    Topics: Geosciences
    Published by Geological Society of London
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  • 10
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    Sustainable Minerals Operations in the Developing World: introduction (2005)
    Geological Society of London
    Details
    Publication Date: 2005-01-01
    Print ISSN: 0305-8719
    Electronic ISSN: 2041-4927
    Topics: Geosciences
    Published by Geological Society of London
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