Search Results - (Author, Cooperation:H. Jasper)

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  1. 1
    H. Deng ; A. A. Gerencser ; H. Jasper
    Nature Publishing Group (NPG)
    Published 2015
    Staff View
    Publication Date:
    2015-12-04
    Publisher:
    Nature Publishing Group (NPG)
    Print ISSN:
    0028-0836
    Electronic ISSN:
    1476-4687
    Topics:
    Biology
    Chemistry and Pharmacology
    Medicine
    Natural Sciences in General
    Physics
    Keywords:
    Animals ; Calcium/*metabolism ; Cell Proliferation/drug effects ; Cytosol/chemistry ; Diet ; Drosophila melanogaster/*cytology/drug effects/metabolism ; Glutamic Acid/pharmacology ; Intestines/cytology ; Receptors, Metabotropic Glutamate/metabolism ; *Signal Transduction ; Stem Cells/*cytology/metabolism
    Published by:
    Latest Papers from Table of Contents or Articles in Press
  2. 2
    Latest Papers from Table of Contents or Articles in Press
  3. 3
    Miguel-Aliaga, I., Jasper, H., Lemaitre, B.
    Genetics Society of America (GSA)
    Published 2018
    Staff View
    Publication Date:
    2018-10-05
    Publisher:
    Genetics Society of America (GSA)
    Print ISSN:
    0016-6731
    Topics:
    Biology
    Published by:
    Latest Papers from Table of Contents or Articles in Press
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    Staff View
    ISSN:
    0016-6480
    Source:
    Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics:
    Biology
    Medicine
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
  8. 8
    Kane, Jasper H. ; Finlay, A. C. ; Sobin, B. A.

    Oxford, UK : Blackwell Publishing Ltd
    Published 1950
    Staff View
    ISSN:
    1749-6632
    Source:
    Blackwell Publishing Journal Backfiles 1879-2005
    Topics:
    Natural Sciences in General
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
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    JASPER, H. H. ; RANEY, E. T.

    Urbana, etc. : Periodicals Archive Online (PAO)
    Published 1937
    Articles: DFG German National Licenses
  11. 11
    RANEY, E. T. ; JASPER, H. H.

    Urbana, etc. : Periodicals Archive Online (PAO)
    Published 1937
    Articles: DFG German National Licenses
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    Staff View
    ISSN:
    1432-198X
    Keywords:
    Key words Growth ; Growth factors ; Dislipoproteinemia ; Bone mineral density ; Serum leptin ; Renal transplantation ; Deflazacort
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract  Kidney function, growth velocity, weight/ height ratio, body composition, lipid profile, and bone mass were studied in a randomized, multicenter trial of deflazacort versus methylprednisone in 27 prepubertal patients with kidney transplantation. Methylprednisone (0.20±0.03) was replaced by deflazacort (13 patients, 0.30±0.03 mg/kg per day). After 12 months, creatinine clearance decreased significantly only during methylprednisone therapy. Growth velocity increased only in patients treated with deflazacort from 3.3±0.6 to 5.6±0.5 cm/year. Serum levels of several components of the insulin-like growth factor axis did not change. Weight/height ratio was increased in methylprednisone-treated patients (P〈0.05) and decreased in deflazacort-treated patients (P〈0.005). Lean body mass increased in both groups (P〈0.005). Fat body mass and serum leptin increased only in methylprednisone-treated patients (P〈0.025). Total cholesterol and low-density lipoprotein-cholesterol increased in methylprednisone-treated patients by 9.9% (P〈0.05) and 12.5% (P〈0.025). High-density lipoprotein-cholesterol increased by 21% (P〈0.005) and apolipoprotein B decreased by 11% (P〈0.005) in deflazacort-treated patients. Total skeleton and lumbar spine bone mineral density decreased in both groups, but at 1 year methylprednisone-treated patients had lost 50% more bone. Bone mineral content decreased only in methylprednisone-treated patients (P〈0.01). Our data suggest that substituting deflazacort for maintenance methylprednisone might prevent height loss, excessive bone loss, and fat accumulation; and leads to an improvement in the lipoproteins of these children.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses
  20. 20
    Staff View
    ISSN:
    1432-5233
    Keywords:
    Key words Non-enzymatic glycosylation ; Insulin-like growth factor ; Binding proteins ; Chronic complications ; Diabetes mellitus
    Source:
    Springer Online Journal Archives 1860-2000
    Topics:
    Medicine
    Notes:
    Abstract The possible occurrence of increased non-enzymatic glycosylation of serum insulin-like growth factor binding protein-3 (IGFBP-3) in vivo and the changes that would simultaneously occur in serum levels of IGFBP-3 and insulin-like growth factor-1 (IGF-I) were investigated. We measured levels of IGF-I and IGFBP-3 and the degree of glycation of total serum protein and IGFBP-3, in serum samples obtained from patients with poorly controlled non-insulin-dependent diabetes (type 2) and from age-matched non-diabetic controls. Type 2 diabetic patients had significantly higher glycated serum protein (GlyP) levels. GlyP significantly correlated with age in the control (r = 0.315, P〈0.05) but not in the type 2 diabetes group. Control and diabetic subjects had comparable serum IGF-I levels and in both groups IGF-I levels tended to decrease with age (r = –0.567, P〈0.001 and r = –0.465, P〈0.05 for control and type 2 diabetic subjects, respectively). In the type 2 diabetes group, IGF-I levels showed a negative correlation with serum GlyP values (r = –0.476, P〈0.05). Type 2 diabetic and control patients had comparable serum IGFBP-3 levels, which were significantly higher in diabetic patients in the older age subgroups. A negative correlation was found between IGFBP-3 levels and age in the control (r = –0.705, P〈0.001) and in the type 2 diabetes groups (r = –0.463, P〈0.05). A significant negative correlation was found between IGFBP-3 levels and GlyP in control (r = –0.449, P〈0.002) but not in type 2 diabetic subjects. The mean glycated IGFBP-3 (GlyIGFBP-3) levels were higher in the oldest type 2 diabetic patients. In these patients, GlyIGFBP-3 was negatively associated with IGF-I levels (r = –0.447, P〈0.05). The IGF-I/IGFBP-3 molar ratio was significantly reduced in the 46–60-year-old type 2 diabetic group, whereas the IGF-I/IGFBP-3 ratio was positively and significantly correlated with GlyP levels only in the control group (r = 0.489, P〈0.01). Our results show that: a) increased non-enzymatic glycosylation of IGFBP-3 occurs in vivo; and b) this effect is accompanied by an increase in IGFBP-3 levels. These results suggest that the IGF-I/IGFBP-3 system is another target for the metabolic derangements of type 2 diabetes. Its alterations might play a role in diabetic complications.
    Type of Medium:
    Electronic Resource
    URL:
    Articles: DFG German National Licenses