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  • 1
    Publication Date: 2018
    Description: Inherited retinal degenerations are the leading cause of blindness in the working population. X-linked retinitis pigmentosa (XLRP), caused by mutations in the Retinitis pigmentosa GTPase regulator (RPGR) gene is one of the more severe forms, and female carriers of RPGR mutations have a variable presentation. A retrospective review of twenty-three female RPGR carriers aged between 8 and 76 years old was carried out using fundoscopy, autofluorescence imaging (AF), blue reflectance (BR) imaging and optical coherence tomography (OCT). Confirmation of the genetic mutation was obtained from male relatives or Sanger genetic sequencing. Fundus examination and AF demonstrate phenotypic variability in RPGR carriers. The genetic mutation appears indeterminate of the degree of change. We found four distinct classifications based on AF images to describe RPGR carriers; normal (N) representing normal or near-normal AF appearance (n = 1, 4%); radial (R) pattern reflex without pigmentary retinopathy (n = 14, 61%); focal (F) pigmentary retinopathy (n = 5, 22%) and; male (M) phenotype (n = 3, 13%). The phenotypes were precisely correlated in both eyes (rs = 1.0, p 〈 0.0001). Skewed X-inactivation can result in severely affected carrier females—in some cases indistinguishable from the male pattern and these patients should be considered for RPGR gene therapy. In the cases of the male (M) phenotype where the X-inactivation was skewed, the pattern was similar in both eyes, suggesting that the mechanism is not truly random but may have an underlying genetic basis.
    Electronic ISSN: 2073-4425
    Topics: Biology
    Published by MDPI
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  • 2
    Publication Date: 2016-06-17
    Description: Circulation on the Antarctic continental shelf influence cross-shelf exchange, Antarctic Bottom Water formation, and ocean heat flux to floating ice shelves. The physical processes driving the shelf circulation and its seasonal and interannual variability remain poorly understood. We use a unique time series of repeat hydrographic observations from the Adélie Land continental shelf and a box inverse model to explore the relationship between surface forcing, shelf circulation, cross-shelf exchange, and dense water formation. A wind-driven northwestward coastal current, set up by onshore Ekman transport, dominates the summer circulation. During winter, strong buoyancy loss creates dense shelf water. This dense water flows off the shelf, with a compensating on-shelf flow that is an order of magnitude larger in winter than in summer. The results demonstrate the importance of winter buoyancy loss in driving the shelf circulation and cross-shelf exchange, as well as dense water mass formation.
    Print ISSN: 0094-8276
    Electronic ISSN: 1944-8007
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 3
    Publication Date: 2011-06-14
    Description: Recent studies suggest that the overturning circulation in the Antarctic Circumpolar Current (ACC) region shows a weak sensitivity to overlying wind stress changes, due to balancing of changes in the eddy-induced and Eulerian mean transports. Using an eddy-permitting coupled climate model, we analyze the response of the ACC transport, and associated water mass subduction rates, in response to an idealized poleward shift and intensification of the westerlies. As in previous studies, we find a small increase in the net ACC transport, and a poleward shift in the mean position of the ACC flow. However, the ACC is restructured, with the Subantarctic Front (SAF) and Polar Front (PF) branches shifting poleward by between 0.9° and 2.5° of latitude, resulting in a weaker ACC flow in both the SAF and PF zones. The wind stress anomaly drives a stronger northward Ekman transport of cool surface waters, deepening the winter mixed layer and causing a 12.7 Sv increase in the subduction of Subantarctic Mode Water (SAMW) north of the SAF zone and a 6.5 Sv increase in the subduction of Antarctic Intermediate Water (AAIW) within the SAF and PF zones. Our results suggest that changes in the wind stress restructure the Southern Ocean large-scale circulation, including the flow of the ACC in its primary jets, and that this affects the formation rates of SAMW and AAIW in this complex region.
    Print ISSN: 0094-8276
    Electronic ISSN: 1944-8007
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 4
    Publication Date: 2012-07-29
    Description: Canadian Journal of Forest Research, Volume 0, Issue 0, Page 1577-1586, e-First articles.
    Print ISSN: 0045-5067
    Electronic ISSN: 1208-6037
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition
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  • 5
    Publication Date: 2019
    Description: Abstract Upwelling in the world's strongest current, the Antarctic Circumpolar Current, is thought to be driven by wind stress, surface buoyancy flux, and mixing generated from the interaction between bottom currents and rough topography. However, the impact of localized injection of heat by hydrothermal vents where the Antarctic Circumpolar Current interacts with mid‐ocean ridges remains poorly understood. Here a circumpolar compilation of helium and physical measurements are used to show that while geothermal heat is transferred to the ocean over a broad area by conduction, heat transfer by convection dominates near hydrothermal vents. Buoyant hydrothermal plumes decrease stratification above the vent source and increase stratification to the south, altering the local vertical diffusivity and diapycnal upwelling within 500 m of the sea floor by an order of magnitude. Both the helium tracer and stratification signals induced by hydrothermal input are advected by the flow and influence properties downstream.
    Print ISSN: 0094-8276
    Electronic ISSN: 1944-8007
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 6
    Publication Date: 2000-03-25
    Description: The fly Drosophila melanogaster is one of the most intensively studied organisms in biology and serves as a model system for the investigation of many developmental and cellular processes common to higher eukaryotes, including humans. We have determined the nucleotide sequence of nearly all of the approximately 120-megabase euchromatic portion of the Drosophila genome using a whole-genome shotgun sequencing strategy supported by extensive clone-based sequence and a high-quality bacterial artificial chromosome physical map. Efforts are under way to close the remaining gaps; however, the sequence is of sufficient accuracy and contiguity to be declared substantially complete and to support an initial analysis of genome structure and preliminary gene annotation and interpretation. The genome encodes approximately 13,600 genes, somewhat fewer than the smaller Caenorhabditis elegans genome, but with comparable functional diversity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Adams, M D -- Celniker, S E -- Holt, R A -- Evans, C A -- Gocayne, J D -- Amanatides, P G -- Scherer, S E -- Li, P W -- Hoskins, R A -- Galle, R F -- George, R A -- Lewis, S E -- Richards, S -- Ashburner, M -- Henderson, S N -- Sutton, G G -- Wortman, J R -- Yandell, M D -- Zhang, Q -- Chen, L X -- Brandon, R C -- Rogers, Y H -- Blazej, R G -- Champe, M -- Pfeiffer, B D -- Wan, K H -- Doyle, C -- Baxter, E G -- Helt, G -- Nelson, C R -- Gabor, G L -- Abril, J F -- Agbayani, A -- An, H J -- Andrews-Pfannkoch, C -- Baldwin, D -- Ballew, R M -- Basu, A -- Baxendale, J -- Bayraktaroglu, L -- Beasley, E M -- Beeson, K Y -- Benos, P V -- Berman, B P -- Bhandari, D -- Bolshakov, S -- Borkova, D -- Botchan, M R -- Bouck, J -- Brokstein, P -- Brottier, P -- Burtis, K C -- Busam, D A -- Butler, H -- Cadieu, E -- Center, A -- Chandra, I -- Cherry, J M -- Cawley, S -- Dahlke, C -- Davenport, L B -- Davies, P -- de Pablos, B -- Delcher, A -- Deng, Z -- Mays, A D -- Dew, I -- Dietz, S M -- Dodson, K -- Doup, L E -- Downes, M -- Dugan-Rocha, S -- Dunkov, B C -- Dunn, P -- Durbin, K J -- Evangelista, C C -- Ferraz, C -- Ferriera, S -- Fleischmann, W -- Fosler, C -- Gabrielian, A E -- Garg, N S -- Gelbart, W M -- Glasser, K -- Glodek, A -- Gong, F -- Gorrell, J H -- Gu, Z -- Guan, P -- Harris, M -- Harris, N L -- Harvey, D -- Heiman, T J -- Hernandez, J R -- Houck, J -- Hostin, D -- Houston, K A -- Howland, T J -- Wei, M H -- Ibegwam, C -- Jalali, M -- Kalush, F -- Karpen, G H -- Ke, Z -- Kennison, J A -- Ketchum, K A -- Kimmel, B E -- Kodira, C D -- Kraft, C -- Kravitz, S -- Kulp, D -- Lai, Z -- Lasko, P -- Lei, Y -- Levitsky, A A -- Li, J -- Li, Z -- Liang, Y -- Lin, X -- Liu, X -- Mattei, B -- McIntosh, T C -- McLeod, M P -- McPherson, D -- Merkulov, G -- Milshina, N V -- Mobarry, C -- Morris, J -- Moshrefi, A -- Mount, S M -- Moy, M -- Murphy, B -- Murphy, L -- Muzny, D M -- Nelson, D L -- Nelson, D R -- Nelson, K A -- Nixon, K -- Nusskern, D R -- Pacleb, J M -- Palazzolo, M -- Pittman, G S -- Pan, S -- Pollard, J -- Puri, V -- Reese, M G -- Reinert, K -- Remington, K -- Saunders, R D -- Scheeler, F -- Shen, H -- Shue, B C -- Siden-Kiamos, I -- Simpson, M -- Skupski, M P -- Smith, T -- Spier, E -- Spradling, A C -- Stapleton, M -- Strong, R -- Sun, E -- Svirskas, R -- Tector, C -- Turner, R -- Venter, E -- Wang, A H -- Wang, X -- Wang, Z Y -- Wassarman, D A -- Weinstock, G M -- Weissenbach, J -- Williams, S M -- WoodageT -- Worley, K C -- Wu, D -- Yang, S -- Yao, Q A -- Ye, J -- Yeh, R F -- Zaveri, J S -- Zhan, M -- Zhang, G -- Zhao, Q -- Zheng, L -- Zheng, X H -- Zhong, F N -- Zhong, W -- Zhou, X -- Zhu, S -- Zhu, X -- Smith, H O -- Gibbs, R A -- Myers, E W -- Rubin, G M -- Venter, J C -- P50-HG00750/HG/NHGRI NIH HHS/ -- U54 HG003273/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2000 Mar 24;287(5461):2185-95.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Celera Genomics, 45 West Gude Drive, Rockville, MD 20850, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/10731132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Transport/genetics ; Chromatin/genetics ; Cloning, Molecular ; Computational Biology ; Contig Mapping ; Cytochrome P-450 Enzyme System/genetics ; DNA Repair/genetics ; DNA Replication/genetics ; Drosophila melanogaster/*genetics/metabolism ; Euchromatin ; Gene Library ; Genes, Insect ; *Genome ; Heterochromatin/genetics ; Insect Proteins/chemistry/genetics/physiology ; Nuclear Proteins/genetics ; Protein Biosynthesis ; *Sequence Analysis, DNA ; Transcription, Genetic
    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
    Publication Date: 2008-10-22
    Description: The lymphatic system plays a key role in tissue fluid regulation and tumour metastasis, and lymphatic defects underlie many pathological states including lymphoedema, lymphangiectasia, lymphangioma and lymphatic dysplasia. However, the origins of the lymphatic system in the embryo, and the mechanisms that direct growth of the network of lymphatic vessels, remain unclear. Lymphatic vessels are thought to arise from endothelial precursor cells budding from the cardinal vein under the influence of the lymphatic hallmark gene Prox1 (prospero homeobox 1; ref. 4). Defects in the transcription factor gene SOX18 (SRY (sex determining region Y) box 18) cause lymphatic dysfunction in the human syndrome hypotrichosis-lymphoedema-telangiectasia, suggesting that Sox18 may also play a role in lymphatic development or function. Here we use molecular, cellular and genetic assays in mice to show that Sox18 acts as a molecular switch to induce differentiation of lymphatic endothelial cells. Sox18 is expressed in a subset of cardinal vein cells that later co-express Prox1 and migrate to form lymphatic vessels. Sox18 directly activates Prox1 transcription by binding to its proximal promoter. Overexpression of Sox18 in blood vascular endothelial cells induces them to express Prox1 and other lymphatic endothelial markers, while Sox18-null embryos show a complete blockade of lymphatic endothelial cell differentiation from the cardinal vein. Our findings demonstrate a critical role for Sox18 in developmental lymphangiogenesis, and suggest new avenues to investigate for therapeutic management of human lymphangiopathies.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Francois, Mathias -- Caprini, Andrea -- Hosking, Brett -- Orsenigo, Fabrizio -- Wilhelm, Dagmar -- Browne, Catherine -- Paavonen, Karri -- Karnezis, Tara -- Shayan, Ramin -- Downes, Meredith -- Davidson, Tara -- Tutt, Desmond -- Cheah, Kathryn S E -- Stacker, Steven A -- Muscat, George E O -- Achen, Marc G -- Dejana, Elisabetta -- Koopman, Peter -- England -- Nature. 2008 Dec 4;456(7222):643-7. doi: 10.1038/nature07391. Epub 2008 Oct 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland 4072, Australia.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18931657" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; *Cell Differentiation ; Cell Movement ; Cells, Cultured ; Edema/genetics ; Endothelial Cells/cytology/metabolism ; Ephrin-B2/genetics ; Female ; Gene Expression Regulation, Developmental ; Homeodomain Proteins/genetics ; Hypotrichosis/genetics ; Lymphangiogenesis ; Lymphatic Vessels/*cytology/*embryology/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Promoter Regions, Genetic/genetics ; SOXF Transcription Factors/deficiency/genetics/*metabolism ; Telangiectasis/genetics ; Tumor Suppressor Proteins/genetics ; Vascular Endothelial Growth Factor Receptor-3/genetics ; Veins/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2011-12-16
    Description: Mammalian metabolism is highly circadian and major hormonal circuits involving nuclear hormone receptors display interlinked diurnal cycling. However, mechanisms that logically explain the coordination of nuclear hormone receptors and the clock are poorly understood. Here we show that two circadian co-regulators, cryptochromes 1 and 2, interact with the glucocorticoid receptor in a ligand-dependent fashion and globally alter the transcriptional response to glucocorticoids in mouse embryonic fibroblasts: cryptochrome deficiency vastly decreases gene repression and approximately doubles the number of dexamethasone-induced genes, suggesting that cryptochromes broadly oppose glucocorticoid receptor activation and promote repression. In mice, genetic loss of cryptochrome 1 and/or 2 results in glucose intolerance and constitutively high levels of circulating corticosterone, suggesting reduced suppression of the hypothalamic-pituitary-adrenal axis coupled with increased glucocorticoid transactivation in the liver. Genomically, cryptochromes 1 and 2 associate with a glucocorticoid response element in the phosphoenolpyruvate carboxykinase 1 promoter in a hormone-dependent manner, and dexamethasone-induced transcription of the phosphoenolpyruvate carboxykinase 1 gene was strikingly increased in cryptochrome-deficient livers. These results reveal a specific mechanism through which cryptochromes couple the activity of clock and receptor target genes to complex genomic circuits underpinning normal metabolic homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3245818/" 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/PMC3245818/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lamia, Katja A -- Papp, Stephanie J -- Yu, Ruth T -- Barish, Grant D -- Uhlenhaut, N Henriette -- Jonker, Johan W -- Downes, Michael -- Evans, Ronald M -- DK057978/DK/NIDDK NIH HHS/ -- DK062434/DK/NIDDK NIH HHS/ -- DK090188/DK/NIDDK NIH HHS/ -- K01 DK090188/DK/NIDDK NIH HHS/ -- K01 DK090188-01/DK/NIDDK NIH HHS/ -- K01 DK090188-02/DK/NIDDK NIH HHS/ -- P30 CA014195/CA/NCI NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- R37 DK057978-22/DK/NIDDK NIH HHS/ -- U19 DK062434/DK/NIDDK NIH HHS/ -- U19 DK062434-01/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Dec 14;480(7378):552-6. doi: 10.1038/nature10700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gene Expression Laboratory, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA. klamia@scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22170608" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm ; Corticosterone/blood ; Cryptochromes/genetics/*metabolism ; Dexamethasone/pharmacology ; Female ; *Gene Expression Regulation/drug effects ; Glucocorticoids/pharmacology ; Glucose Intolerance/genetics ; HEK293 Cells ; Humans ; Liver/enzymology/metabolism ; Mice ; Phosphoenolpyruvate Carboxykinase (GTP)/blood/metabolism ; Receptors, Glucocorticoid/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 9
    Publication Date: 2015-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, Jae Myoung -- Jonker, Johan W -- Ahmadian, Maryam -- Goetz, Regina -- Lackey, Denise -- Osborn, Olivia -- Huang, Zhifeng -- Liu, Weilin -- Yoshihara, Eiji -- van Dijk, Theo H -- Havinga, Rick -- Fan, Weiwei -- Yin, Yun-Qiang -- Yu, Ruth T -- Liddle, Christopher -- Atkins, Annette R -- Olefsky, Jerrold M -- Mohammadi, Moosa -- Downes, Michael -- Evans, Ronald M -- P01 HL088093/HL/NHLBI NIH HHS/ -- P42 ES010337/ES/NIEHS NIH HHS/ -- R01 DE013686/DE/NIDCR NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- England -- Nature. 2015 Apr 16;520(7547):388. doi: 10.1038/nature14304. Epub 2015 Mar 4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25739500" target="_blank"〉PubMed〈/a〉
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2014-07-22
    Description: Fibroblast growth factor 1 (FGF1) is an autocrine/paracrine regulator whose binding to heparan sulphate proteoglycans effectively precludes its circulation. Although FGF1 is known as a mitogenic factor, FGF1 knockout mice develop insulin resistance when stressed by a high-fat diet, suggesting a potential role in nutrient homeostasis. Here we show that parenteral delivery of a single dose of recombinant FGF1 (rFGF1) results in potent, insulin-dependent lowering of glucose levels in diabetic mice that is dose-dependent but does not lead to hypoglycaemia. Chronic pharmacological treatment with rFGF1 increases insulin-dependent glucose uptake in skeletal muscle and suppresses the hepatic production of glucose to achieve whole-body insulin sensitization. The sustained glucose lowering and insulin sensitization attributed to rFGF1 are not accompanied by the side effects of weight gain, liver steatosis and bone loss associated with current insulin-sensitizing therapies. We also show that the glucose-lowering activity of FGF1 can be dissociated from its mitogenic activity and is mediated predominantly via FGF receptor 1 signalling. Thus we have uncovered an unexpected, neomorphic insulin-sensitizing action for exogenous non-mitogenic human FGF1 with therapeutic potential for the treatment of insulin resistance and type 2 diabetes.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4184286/" 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/PMC4184286/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suh, Jae Myoung -- Jonker, Johan W -- Ahmadian, Maryam -- Goetz, Regina -- Lackey, Denise -- Osborn, Olivia -- Huang, Zhifeng -- Liu, Weilin -- Yoshihara, Eiji -- van Dijk, Theo H -- Havinga, Rick -- Fan, Weiwei -- Yin, Yun-Qiang -- Yu, Ruth T -- Liddle, Christopher -- Atkins, Annette R -- Olefsky, Jerrold M -- Mohammadi, Moosa -- Downes, Michael -- Evans, Ronald M -- DE13686/DE/NIDCR NIH HHS/ -- DK-033651/DK/NIDDK NIH HHS/ -- DK-063491/DK/NIDDK NIH HHS/ -- DK-074868/DK/NIDDK NIH HHS/ -- DK057978/DK/NIDDK NIH HHS/ -- DK090962/DK/NIDDK NIH HHS/ -- ES010337/ES/NIEHS NIH HHS/ -- HL088093/HL/NHLBI NIH HHS/ -- HL105278/HL/NHLBI NIH HHS/ -- P01 DK054441/DK/NIDDK NIH HHS/ -- P01 DK074868/DK/NIDDK NIH HHS/ -- P01 HL088093/HL/NHLBI NIH HHS/ -- P01-DK054441-14A1/DK/NIDDK NIH HHS/ -- P30 DK063491/DK/NIDDK NIH HHS/ -- P42 ES010337/ES/NIEHS NIH HHS/ -- R01 HL105278/HL/NHLBI NIH HHS/ -- R24 DK090962/DK/NIDDK NIH HHS/ -- R37 DK033651/DK/NIDDK NIH HHS/ -- R37 DK057978/DK/NIDDK NIH HHS/ -- T32 DK007494/DK/NIDDK NIH HHS/ -- T32-DK-007494/DK/NIDDK NIH HHS/ -- U54 HD012303/HD/NICHD NIH HHS/ -- U54-HD-012303-25/HD/NICHD NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2014 Sep 18;513(7518):436-9. doi: 10.1038/nature13540. Epub 2014 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA [2]. ; 1] Center for Liver, Digestive and Metabolic Diseases, Departments of Pediatrics and Laboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands [2]. ; Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA. ; Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA. ; Department of Medicine, Division of Endocrinology and Metabolism, University of California at San Diego, La Jolla, California 92093, USA. ; 1] Department of Biochemistry and Molecular Pharmacology, New York University School of Medicine, New York, New York 10016, USA [2] School of Pharmacy, Wenzhou Medical University, Wenzhou, Zhejiang 325035, China. ; Center for Liver, Digestive and Metabolic Diseases, Departments of Pediatrics and Laboratory Medicine, University of Groningen, University Medical Center Groningen, Hanzeplein 1, 9713 GZ Groningen, The Netherlands. ; The Storr Liver Unit, Westmead Millennium Institute and University of Sydney, Westmead Hospital, Westmead, New South Wales 2145, Australia. ; 1] Gene Expression Laboratory, Salk Institute for Biological Studies, La Jolla, California 92037, USA [2] Howard Hughes Medical Institute, Salk Institute for Biological Studies, La Jolla, California 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25043058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; Body Weight/drug effects ; Diabetes Mellitus, Experimental/drug therapy/metabolism ; Diabetes Mellitus, Type 2/metabolism ; Diet, High-Fat ; Dose-Response Relationship, Drug ; Fibroblast Growth Factor 1/administration & dosage/adverse effects/*pharmacology ; Glucose/*metabolism ; Glucose Tolerance Test ; Humans ; Insulin/*metabolism ; Insulin Resistance ; Liver/drug effects/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Obese ; Mitogens/pharmacology ; Muscle, Skeletal/drug effects/metabolism ; Receptor, Fibroblast Growth Factor, Type 1/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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