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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    The @journal of physical chemistry 〈Washington, DC〉 82 (1978), S. 1947-1952 
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of chemical & engineering data 28 (1983), S. 287-293 
    ISSN: 1520-5134
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology , Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] The phosphatidylinositol-3-OH-kinase (PI(3)K) effector protein kinase B (refs 1, 2) regulates certain insulin-responsive genes,, but the transcription factors regulated by protein kinase B have yet to be identified. Genetic analysis in Caenorhabditis elegans has shown that ...
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-198X
    Keywords: Key words: Focal segmental glomerulosclerosis ; Proteinuria ; Race
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. In patients with proteinuria, African-American (AA) ethnicity is reported to be a risk factor for focal segmental glomerulosclereosis (FSGS) and its progression to end-stage renal disease (ESRD). We reviewed our single-center experience to determine the probability of FSGS and its progression to ESRD based on ethnicity and age at presentation in children with proteinuria with or without nephrotic syndrome. Proteinuria without systemic disease or acute glomerulonephritis was the presenting feature in 17% (236/1,403) of children in the renal patient database of Texas Children’s Hospital, Baylor College of Medicine. Histopathological diagnoses were established in 107 of 236 patients (45%). FSGS was identified in 65 patients, accounting for 28% of all patients with proteinuria and 61% of patients who underwent renal biopsy. FSGS was more prevalent in AA (45%) than in non-AA patients (22%) (P=0.001), and AA patients with FSGS were older at presentation (12.7±4.4 years) than non-AA patients (5.6±4.6 years) (P〈0.001). Among patients who underwent renal biopsy, increasing age at presentation increased the probability of having FSGS in AA but not non-AA patients (P=0.04). Five-year actuarial renal survival of FSGS was worse in AA (8%) than in non-AA patients (31%) (P=0.01). These data suggest an increased risk and worse outcome of FSGS in AA compared with non-AA children.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-198X
    Keywords: Growth ; Growth failure ; Renal failure ; Growth hormone ; Insulin-like growth factor ; Insulin-like growth factor binding proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Children with chronic renal failure (CRF) often fail to attain an adult height consistent with their genetic potential. The growth hormone (GH)/insulin-like growth factor (IGF)/growth plate chondrocyte axis has been intensively studied in these children to determine the basis for this growth failure. Evidence suggests that hepatic GH resistance results in deficient expression of IGF-I. However, serum IGF-I levels are usually normal and it is IGF-I action on target tissues which is inhibited, possibly by the presence of excess high-affinity IGF binding proteins (IGFBPs) in CRF serum. In this paper we evaluate the roles of IGFBP-1, -2, and -3 as growth inhibitors in CRF children. The data support a role for each of these IGFBPs as growth inhibitors. Currently, IGFBP-1 meets most criteria expected of a growth inhibitor, but IGFBP-2 and -3 will likely also meet these criteria and may well be important contributors to the growth failure of CRF. Ultimately, many or all of the six IGFBPs may be found to contribute to the excess high-affinity IGF binding sites which are a hallmark of CRF serum and are possible contributors to the growth failure of CRF children.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-198X
    Keywords: Key words: Insulin-like growth factor ; Insulin-like growth factor binding protein ; Chronic renal failure ; Peritoneal dialysate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract .Serum insulin-like growth factors (IGFs), which circulate bound to specific IGF binding proteins (IGFBPs), must exit the intravascular space before acting on target tissues. Little is known about the nature of IGF/IGFBPs in extravascular fluids of patients with chronic renal failure (CRF). Peritoneal dialysate (PD) was studied since, after a short incubation, PD contains proteins which have entered an extravascular space; thus, IGF/IGFBP forms in PD are more likely than serum forms to interact with target tissues. IGF-I and IGF-II, and IGFBPs 1 – 4, were readily identified by specific immunoassays and/or 125iodine-IGF ligand blotting of simultaneously obtained PD and serum samples from seven CRF children; IGFBP-3 was a major IGFBP in PD as in serum. Where quantitated, IGF and IGFBP levels in PD were approximately 10% of serum concentrations. After separation of PD and serum by size-exclusion chromatography, serum had more IGFBP-3 in 150-kilodalton (kDa) than 35-kDa fractions, while PD had far less IGFBP-3 in 150-kDa than 35-kDa fractions. Immunoblot studies revealed a major 29-kDa IGFBP-3 fragment, in addition to intact 41- and 38-kDa IGFBP-3 forms, in PD and CRF serum; the 29-kDa form predominated in the 35-kDa PD fractions. These data suggest that the 29-kDa fragment is the IGFBP-3 form most likely to modulate IGF effects on target tissues of CRF individuals.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-198X
    Keywords: Key words: Growth ; Growth failure ; Renal failure ; Growth hormone ; Insulin-like growth factor ; Insulin-like growth factor binding proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Children with chronic renal failure (CRF) often fail to attain an adult height consistent with their genetic potential. The growth hormone (GH)/insulin-like growth factor (IGF)/growth plate chondrocyte axis has been intensively studied in these children to determine the basis for this growth failure. Evidence suggests that hepatic GH resistance results in deficient expression of IGF-I. However, serum IGF-I levels are usually normal and it is IGF-I action on target tissues which is inhibited, possibly by the presence of excess high-affinity IGF binding proteins (IGFBPs) in CRF serum. In this paper we evaluate the roles of IGFBP-1, -2, and -3 as growth inhibitors in CRF children. The data support a role for each of these IGFBPs as growth inhibitors. Currently, IGFBP-1 meets most criteria expected of a growth inhibitor, but IGFBP-2 and -3 will likely also meet these criteria and may well be important contributors to the growth failure of CRF. Ultimately, many or all of the six IGFBPs may be found to contribute to the excess high-affinity IGF binding sites which are a hallmark of CRF serum and are possible contributors to the growth failure of CRF children.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Pediatric nephrology 2 (1988), S. 425-430 
    ISSN: 1432-198X
    Keywords: Growth hormone therapy ; Malnutrition ; Renal failure ; Growth
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We examined the effects of methionylhuman growth hormone (met-hGH) and malnutrition on the growth of 5/6 nephrectomized rats and sham-operated controls. One group of shamoperated rats (PFS) was pair-fed with a group of nephrectomized rats in renal failure (RF); another group of sham-operated rats was fed ad libitum (ALS), and a final group of rats with renal failure (RF-GH) was treated with 4 IU/day met-hGH. After 4 weeks, RF-GH rats gained 12.3±1.7 cm in length; this was more than the 10.2±1.2 cm gain of RF rats (P〈0.05). Ingested food was converted into weight gain more efficiently by RF-GH rats than RF rats (267±26 vs 235±38 mg weight gain/g food intake,P〈0.05). RF-GH rats also gained more weight (122±25 g) than RF rats (98±27 g), but this difference was not significant (0.05〈P〈0.1). Insulin-like growth factor (IGF)-I, glucose and insulin levels were not different between RF and RF-GH rats. Food intake of RF and PFS rats was 64% of ALS intake and was associated with poor gains in weight and length by the PFS and RF groups (relative weight and length gains were ALS〉PFS〉RF,P〈0.05 for all comparisons); this suggests that the poor growth of RF rats when compared with PFS rats was due to factors other, than food intake. Serum IGF-I levels of 771±249 ng/ml in PFS rats were lower than levels of 1109±253 ng/ml found in the ALS group (P〈0.05); this is consistent with the malnourished state of PFS rats. Serum IGF-I levels in RF rats (950±236 ng/ml) were not different from ALS or PFS levels despite the fact that RF rats gained less weight and length than either the ALS or PFS rats. We conclude that RF rats increase in length, use ingested calories more efficiently, and fail to develop marked insulin resistance when treated with met-hGH. We find that, in addition to poor food intake, other factors contribute to growth failure in this model of renal failure. Finally, we find that RF rats have normal levels of IGF-I, suggesting that low IGF-I levels are not a major cause of growth failure in rats with renal failure.
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Breast cancer research and treatment 18 (1991), S. 3-10 
    ISSN: 1573-7217
    Keywords: estradiol stimulation ; human breast cancer cells ; insulin-like growth factors ; insulin-like growth factor binding proteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The insulin-like growth factors (IGFs) are potent mitogens for some breast cancer cell lines. Recent evidence suggests that IGF-induced mitogenesis may be influenced by specific IGF binding proteins (IGFBPs). In this study, breast cancer cell lines were examined for IGFBP protein and mRNA expression. Western ligand blot examination of conditioned media from breast cancer cell lines suggested that the IGFBP protein expression was heterogeneous. Although all breast cancer cell lines expressed a 24kDa binding protein, MCF-7, an estrogen receptor positive (ER+) cell line, expressed a IGFBP compatible with reported sizes for IGFBP-2. Estrogen receptor negative (ER−) cells (MDA-MD-231, Hs578T) secreted IGFBPs consistent with sizes reported for IGFBP-1 and -3. Examination of mRNA expression supported these findings; IGFBP-2 was seen in all (4/4) ER+ cell lines while high levels of IGFBP-3 were found in ER− cell lines (3/5), although lower levels of IGFBP-3 mRNA could be found in some ER+ cell lines. In MCF-7 cells, steady state levels of IGFBP-3 mRNA were decreased by estradiol, while IGFBP-2 mRNA levels were slightly increased. These data suggest that IGFBP expression by breast cancer cells is heterogeneous, that the pattern of IGFBP expression is different between ER+ and ER− cell lines, and that in ER+ cells IGFBP mRNA may be regulated by estrogens. Thus, the IGFBPs may play an important role in mediating the mitogenic response of breast cancer cells to the IGFs.
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