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Chong Sun, Liqin Wang, Sidong Huang, Guus J J E Heynen, Anirudh Prahallad, Caroline Robert, John Haanen, Christian Blank, Jelle Wesseling, Stefan M Willems, Davide Zecchin, Sebastijan Hobor, Prashanth K Bajpe, Cor Lieftink, Christina Mateus, Stephan Vagner, Wipawadee Grernrum, Ingrid Hofland, Andreas Schlicker, Lodewyk F A Wessels, Roderick L Beijersbergen, Alberto Bardelli, Federica Di Nicolantonio, Alexander M M Eggermont, Rene Bernards
Treatment of BRAF(V600E) mutant melanoma by small molecule drugs that target the BRAF or MEK kinases can be effective, but resistance develops invariably. In contrast, colon cancers that harbour the same BRAF(V600E) mutation are intrinsically resistant to BRAF inhibitors, due to feedback activation of the epidermal growth factor receptor (EGFR). Here we show that 6 out of 16 melanoma tumours analysed acquired EGFR expression after the development of resistance to BRAF or MEK inhibitors. Using a chromatin-regulator-focused short hairpin RNA (shRNA) library, we find that suppression of sex determining region Y-box 10 (SOX10) in melanoma causes activation of TGF-β signalling, thus leading to upregulation of EGFR and platelet-derived growth factor receptor-β (PDGFRB), which confer resistance to BRAF and MEK inhibitors...
April 3, 2014: Nature
Crystal Johnson-Holiday, Rajesh Singh, Erica L Johnson, William E Grizzle, James W Lillard, Shailesh Singh
BACKGROUND: Chemotherapy heavily relies on apoptosis to kill breast cancer (BrCa) cells. Many breast tumors respond to chemotherapy, but cells that survive this initial response gain resistance to subsequent treatments. This leads to aggressive cell variants with an enhanced ability to migrate, invade and survive at secondary sites. Metastasis and chemoresistance are responsible for most cancer-related deaths; hence, therapies designed to minimize both are greatly needed. We have recently shown that CCR9-CCL25 interactions promote BrCa cell migration and invasion, while others have shown that this axis play important role in T cell survival...
2011: World Journal of Surgical Oncology
Patricia K Duffner, Verne S Caviness, Richard W Erbe, Marc C Patterson, Kirk R Schultz, David A Wenger, Chester Whitley
Krabbe disease (globoid cell leukodystrophy) is an autosomal recessive disorder of white matter resulting from deficiency of galactosylceramide beta-galactosidase (GALC) and the consequent accumulation of galactosylceramide and psychosine. Although most patients present within the first 6 months of life, i.e., the early infantile or "classic" phenotype, others present later in life including in adolescence and adulthood. The only available treatment for infants with early infantile Krabbe disease is hematopoietic cell transplantation (HCT), typically using umbilical cord blood...
June 2009: Genetics in Medicine: Official Journal of the American College of Medical Genetics
S Chaleff, M Otto, R C Barfield, T Leimig, R Iyengar, J Martin, M Holiday, J Houston, T Geiger, V Huppert, R Handgretinger
BACKGROUND: We sought to develop a method for the clinical large-scale depletion of alphabeta T lymphocytes from mobilized peripheral stem cells, which would allow the allogeneic transplantation of a graft enriched for stem cells, natural killer (NK) cells and gammadelta T lymphocytes. METHODS: Therefore, we obtained mononuclear cells from either mobilized or non-mobilized healthy adult volunteer donors and incubated the cells with a biotinylated anti-alphabeta T-cell Ab and subsequently with an anti-biotin Ab conjugated with magnetic microbeads...
2007: Cytotherapy
R J Miller, C W Ragsdale
No abstract text is available yet for this article.
November 2000: Nature Neuroscience
H Alkadhi, M Tschöp, A Marschang, I Langenmayer, H E Feucht, C J Strasburger
HISTORY AND CLINICAL FINDINGS: One week after returning from a two-week holiday in Sri Lanka a 35-year-old man started to have recurrent bouts of fever, up to 39.2 degrees C, as well as pain over the left upper abdomen, the back of the right thorax and bilateral pain on pressure with swelling of both breasts. He went to the Tropical Institute in Munich to have malaria excluded. There signs of cholestasis were noted and sonography revealed multiple round foci in the liver. As he had lost 10 kg in 3 weeks he was admitted to a medical unit for further tests...
January 30, 1998: Deutsche Medizinische Wochenschrift
S Shetty, A Kumar, A R Johnson, S Pueblitz, D Holiday, G Raghu, S Idell
Binding of urokinase-type plasminogen activator (uPA) to a specific receptor (uPAR) on human lung fibroblasts enables it to regulate cellular proteolysis and remodeling of the extracellular matrix. Binding studies with radiolabeled uPA indicated that both normal and fibrotic lung fibroblasts express the receptor, but cells from fibrotic tissues bound significantly more uPA (P < 0.001). Phorbol myristate acetate, lipopolysaccharide, transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha) increased uPA binding and plasminogen activation at the cell surface, with a greater maximal effect on fibrotic than on normal fibroblasts...
July 1996: American Journal of Respiratory Cell and Molecular Biology
D E Griffith, A R Johnson, A Kumar, D B Holiday, S Idell
Fibrin deposition within the pleural space may influence repair following pleural injury. Although the mesothelial surface can organize fibrin, the contribution of pleural mesothelial cells to pleural repair is unknown. During coagulation thrombin cleaves Fibrinopeptide A (FPA, A alpha 1-16) and fibrinopeptide B (FPB) from the A alpha and B beta chains of fibrinogen to generate fibrin monomer. Since these peptides are mitogenic for human fibroblasts, we considered that they might stimulate replication of human pleural mesothelial cells (HPMC)...
May 1, 1994: Thrombosis Research
S Idell, A Kumar, C Zwieb, D Holiday, K B Koenig, A R Johnson
The epithelial lining of the airways is subject to injury through several processes, including infections, bronchiolitis, and fume exposures. Because airway fibrin deposition influences the course of local injury, we examined how two inflammatory cytokines influenced fibrin formation and clearance in human tracheal epithelial cells (TEC). TEC were treated with transforming growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha). TNF-alpha increased release of tissue factor (TF)-related procoagulant activity that, through generation of factor Xa, promotes assembly of the prothrombinase complex at the cell surface...
December 1994: American Journal of Physiology
A O Azghani, I Williams, D B Holiday, A R Johnson
Adherence through carbohydrate-binding adhesins is an early step in colonization of the lung by gram-negative organisms, and because published data indicate that binding involves mannose groups, we tested the ability of a beta-linked acetyl-mannan (acemannan) to inhibit adherence of Pseudomonas aeruginosa to cultures of human lung epithelial cells. Adherence of radiolabelled P.aeruginosa to A549 cells (a type II-like pneumocyte line) increased linearly with the duration of the incubation. Acemannan inhibited adherence of bacteria, and the extent of inhibition was related to the concentration of the mannan...
February 1995: Glycobiology
S Idell, C Zwieb, J Boggaram, D Holiday, A R Johnson, G Raghu
Fibrin gels form within the alveolar and interstitial compartments of the injured lung, and fibroblasts invade and facilitate organization of these transitional gels. We studied the effects of transforming growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha) on fibrinolytic and procoagulant activities of human lung fibroblasts (HLF) to determine their capacity to regulate pulmonary fibrin deposition. Fibrinolytic activity of cell lysates and media (n = 6 HLF cultures) were uniformly depressed by TGF-beta or TNF-alpha...
October 1992: American Journal of Physiology
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