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  • 1
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Clinical & experimental allergy 34 (2004), S. 0 
    ISSN: 1365-2222
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background IL-10 plays an immunosuppressive role in inflammatory responses. Increased plasma levels of IL-10 have been detected in patients under glucocorticoid (GC) therapy, indicating that steroids may exert their suppressive effect, in part, by increasing IL-10 production.Objectives The aim was to define possible mechanisms by which steroids up-regulate IL-10 production. To this end, we have analysed ex vivo the effect of GCs on the constitutive production of IL-10 by lymphocytes and cells of myeloid origin.Methods Monocytes and T cells were isolated by a Percoll gradient and B cells were purified by rosetting. Protein and mRNA IL-10 levels were determined by ELISA and by Northern blot, respectively.Results Monocytes, but not T or B cells, up-regulated the constitutive production of IL-10 following pre-treatment for at least 12 h with physiological doses of dexamethasone (Dex). Up-regulation of IL-10 occurred at both protein and mRNA levels, probably indicating that the effect of Dex was by incrementing gene transcription. Other steroids had similar outcomes, their effects being dose-related, proportional to the steroid potency and totally reversed by the steroid antagonist RU486. Thus, transcript levels of IL-10 were up-regulated by GCs probably through binding of the GC receptor to its specific glucocorticoid response element sequence in the IL-10 promoter. In contrast to monocytes, differentiated immature macrophages and dendritic cells did not vary their constitutive IL-10 production after pre-treatment with Dex.Conclusion Our results support the fact that steroids up-regulate constitutive IL-10 production by selectively triggering activation signals on monocytes.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1398-9995
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background: An altered production of cytokines has been described in Gleich's syndrome. Our aim was to study the cytokine production at the single-cell level in a patient with Gleich's syndrome and to determine whether it changed during a flare episode. Methods: Blood samples were obtained from a 30-year-old woman diagnosed with Gleich's syndrome before and during the subsequent flare of edema of trunk and arms and weight gain. The major lymphoid subsets (CD4+, CD8+, and CD19+) and natural killer (NK) cells were measured by flow cytometry. Cytokine-producing T cells (IL-2, IFN-γ, and IL-4) were quantified in whole blood by intracellular staining with specific monoclonal antibodies and flow cytometry analysis after polyclonal stimulation with phorbol 12-myristate 13-acetate and ionomycin. Results: Increased numbers of immature CD4+CD8+ T cells and NK cells were observed in peripheral blood during the asymptomatic period. The latter population significantly decreased during the flare. Type-1 cells were decreased in both asymptomatic and, more markedly, during the attack with respect to healthy subjects. Conclusions: The decreased type-1 response demonstrated in this patient might be the basis of the hypereosinophilia of Gleich's syndrome. Besides, the NK cells might play a role in the pathogenesis of these inflammatory episodes.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-2307
    Keywords: Breast carcinoma ; ERBB2 ; E-cadherin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A recent in vitro study has suggested that overexpression of ERBB2 may mediate breast tumour progression and metastasis by inhibiting the transcription of the E-cadherin (E-CD) gene. To test this hypothesis in human breast cancer in vivo, we studied the relationship between the expression of both molecules in 247 breast carcinomas immunohistochemically. Five ductal carcinomas in situ overexpressed ERBB2 and showed preserved E-CD expression. Forty-four of 226 infiltrating ductal carcinomas (19.47%) showed ERBB2 overexpression, and a statistically significant relationship was found between ERBB2 overexpression and high histological grade. E-CD expression was preserved in 111 cases (49.1%) and correlated with the histological grade. However, no significant relationship was found between ERBB2 and E-CD expression. None of the 16 infiltrating lobular carcinomas expressed ERBB2 or E-CD. These observations in different histological types of breast carcinoma strongly argue against a role for ERBB2 as a transcriptional regulator of E-CD expression in most human breast carcinomas in vivo.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford [u.a.] : International Union of Crystallography (IUCr)
    Acta crystallographica 55 (1999), S. 0-0 
    ISSN: 1600-5759
    Source: Crystallography Journals Online : IUCR Backfile Archive 1948-2001
    Topics: Chemistry and Pharmacology , Geosciences , Physics
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-0428
    Keywords: Gliclazide ; skeletal muscle ; glucose uptake ; hindquarter perfusion ; insulin ; ATP-sensitive ; K+ channels ; diazoxide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We studied the effect of gliclazide, a second-generation sulphonylurea, on rat skeletal muscle glucose uptake using perfused hindquarter muscle preparations. Gliclazide at concentrations of 10 to 1000 Μg/ml increased (p〈0.05) the basal glucose uptake. The effect of gliclazide on glucose uptake was immediate and dose-dependent, reaching a plateau at a concentration of 300 Μg/ml; the half-maximal effect was obtained between 25 and 50 Μg/ml. The glucose uptake stimulated by gliclazide (300–1000 Μg/ ml) did not differ from that achieved by 10−9 mol/l insulin, and was lower (p〈0.05) than that obtained with 10−7 mol/l insulin. The combination of gliclazide (300 Μg/ml) and 10−9 mol/l insulin produced an increase in glucose uptake (7.7±0.6 Μmol · g−1 · h−1, n=8, mean±SEM) which was higher (p〈0.05) than that achieved with 10−9 mol/l insulin (5.6±0.7 Μmol · g−1 · h−1, n=11) and not different from that obtained with 10−7 mol/l insulin (9.8±1.0 Μmol · g−1 · h−1, n=11). Diazoxide (100 Μmol/l), an ATP-sensitive K+ channel opener, reversed the stimulatory effect of gliclazide (100 Μg/ml) on muscle glucose uptake from 3.1±0.4 to 0.5±0.2 Μmol · g−1 · h−1, (n=7, p〈0.001). The addition of diazoxide prior to gliclazide into the perfusion medium blocked the gliclazide-induced glucose uptake by the hindquarter muscle preparations. In conclusion, gliclazide alone has an immediate stimulatory effect on glucose uptake by skeletal muscle and together with insulin has an additive effect on muscle glucose uptake. The effect of gliclazide on muscle glucose uptake seems to be due to the inhibition of ATP-sensitive K+ channels.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-0428
    Keywords: Magnesium ; insulin receptors ; tyrosine kinase ; skeletal muscle ; insulin secretion ; glucose disposal ; GLUT 4
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of magnesium deficiency on glucose disposal, glucose-stimulated insulin secretion and insulin action on skeletal muscle was investigated in rats which were fed a low magnesium-containing diet for 4 days. Control rats were fed a standard diet. Compared to the control rats, the rats fed with low magnesium diet presented: 1) lower serum magnesium levels (0.45±0.02 vs 0.78±0.01 mmol/l, p〈0.001), 2) higher basal serum glucose (6.8±0.2 vs 5.5±0.2 mmol/l, p〈0.05) and similar basal serum insulin, 3) 40% reduction (p〈0.001) in the glucose disappearance rate after its i.v. administration, and 4) 45% reduction (p〈0.05) in the glucose-stimulated insulin secretion. The insulin action upon the glucose uptake by skeletal muscle was determined by means of hindquarter perfusions. Compared with control rats, magnesium-deficient rats presented: 1) normal basal glucose uptake, 2) lower stimulatory effect on the glucose uptake by insulin at the concentrations of 5×10−10 mol/l (3.0±0.9 vs 5.4±0.6, p〈0.05) and 5×10−9mol/l (6.3±0.5 vs 8.0±0.5, p〈0.05), 3) normal glucose uptake at a maximal insulin concentration of 1×10−7 mol/l, and 4) 50% reduction in the insulin sensitivity (ED50: 1.3±0.3 vs 0.55±0.1 mol/l, p〈0.05). In partially purified insulin receptors prepared from gastrocnemius muscle, 125I-insulin binding was similar in both groups of rats. However, the autophosphorylation of the Β-subunit of the insulin receptor was significantly reduced by 50% in magnesium-deficient rats and the tyrosine kinase activity of insulin receptors toward the exogenous substrate Poly Glu4: Tyr 1 was also reduced (p〈0.05) by hypomagnesaemia. The abundance of the insulin-sensitive glucose transporter protein (muscle/fat GLUT4), measured by Western blot analysis using polyclonal antisera, was similar in muscles of control and hypomagnesaemic rats. These findings indicate that hypomagnesaemia has a deleterious effect on glucose metabolism due to an impairment of both insulin secretion and action. The insulin resistance observed in skeletal muscle of magnesium-deficient rats may be attributed, at least in part, to a defective tyrosine kinase activity of insulin receptors.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0428
    Keywords: Key words Magnesium ; insulin receptors ; tyrosine kinase ; skeletal muscle ; insulin secretion ; glucose disposal ; GLUT 4.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of magnesium deficiency on glucose disposal, glucose-stimulated insulin secretion and insulin action on skeletal muscle was investigated in rats which were fed a low magnesium-containing diet for 4 days. Control rats were fed a standard diet. Compared to the control rats, the rats fed with low magnesium diet presented: 1) lower serum magnesium levels (0.45 ± 0.02 vs 0.78 ± 0.01 mmol/l, p 〈 0.001), 2) higher basal serum glucose (6.8 ± 0.2 vs 5.5 ± 0.2 mmol/l, p 〈 0.05) and similar basal serum insulin, 3) 40 % reduction (p 〈 0.001) in the glucose disappearance rate after its i. v. administration, and 4) 45 % reduction (p 〈 0.05) in the glucose-stimulated insulin secretion. The insulin action upon the glucose uptake by skeletal muscle was determined by means of hindquarter perfusions. Compared with control rats, magnesium-deficient rats presented: 1) normal basal glucose uptake, 2) lower stimulatory effect on the glucose uptake by insulin at the concentrations of 5 × 10−10 mol/l (3.0 ± 0.9 vs 5.4 ± 0.6, p 〈 0.05) and 5 × 10−9 mol/l (6.3 ± 0.5 vs 8.0 ± 0.5, p 〈 0.05), 3) normal glucose uptake at a maximal insulin concentration of 1 × 10−7 mol/l, and 4) 50 % reduction in the insulin sensitivity (ED50: 1.3 ± 0.3 vs 0.55 ± 0.1 mol/l, p 〈 0.05). In partially purified insulin receptors prepared from gastrocnemius muscle, 125I-insulin binding was similar in both groups of rats. However, the autophosphorylation of the β -subunit of the insulin receptor was significantly reduced by 50 % in magnesium-deficient rats and the tyrosine kinase activity of insulin receptors toward the exogenous substrate Poly Glu4: Tyr 1 was also reduced (p 〈 0.05) by hypomagnesaemia. The abundance of the insulin-sensitive glucose transporter protein (muscle/fat GLUT4), measured by Western blot analysis using polyclonal antisera, was similar in muscles of control and hypomagnesaemic rats. These findings indicate that hypomagnesaemia has a deleterious effect on glucose metabolism due to an impairment of both insulin secretion and action. The insulin resistance observed in skeletal muscle of magnesium-deficient rats may be attributed, at least in part, to a defective tyrosine kinase activity of insulin receptors. [Diabetologia (1995) 38: 1262–1270]
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1436-6215
    Keywords: Key words Long chain polyunsaturated fatty acids – peroxidation – vitamin E – weanling rats
    Source: Springer Online Journal Archives 1860-2000
    Topics: Agriculture, Forestry, Horticulture, Fishery, Domestic Science, Nutrition , Medicine
    Notes: Summary Background: Tissue 10:4(n-6) and 22:6(n-3) status have been correlated with neonatal development and growth. Artificial formulas for neonates have been supplemented with long chain polyunsaturated fatty acids (LCP) from animal and marine sources which may enhance sensitivity of cellular membranes to oxidative damage. Diet-derived antioxidants like vitamin E play a key role in the protection of tissue lipids against oxidation. Aim of the study: We seek to determine the influence of dietary vitamin E on tissue sensitivity to oxidative stress in rats fed for 4 weeks on diets enriched in (n-3) and (n-6) long-chain polyunsaturated fatty acids. Methods: Weanling rats received 10% fat diets that provided 18:1(n-9), 18:2(n-6) and 18:3(n-3) in a similar ratio to that of rat milk (group A), supplemented with fish oil (groups B and B+E) and supplemented with (n-6) and (n-3) LCP from an animal phospholipid concentrate (groups C and C+E). Vitamin E (500 mg vitamin E/kg fat) was added to diets B+E and C+E. Tissue fatty acid content and the activities of catalase, superoxide dismutase, glutathione transferase und glutathione peroxidase in liver and brain were measured. Glutathione status, vitamin E and the production of thiobarbituric acid reactive substances (TBARs) after incubation of erythrocyte, liver and brain lipids with inducers of enzymatic or non-enzymatic lipid peroxidation was measured. Results: Group B registered significantly lower total superoxide dismutase acitvity than group B+. Catalase activity was significantly higher in group C than in group C+E. Hepatic total and reduced glutathione levels were decreased in vitamin E supplemented groups compared to unsupplemented ones. TBARs production in erythrocyte lipids was significantly higher in groups B and C compared to vitamin E supplemented groups B+E and C+E. Conclusions: This study shows that the addition of vitamin E protected erythrocyte and liver microsome lipids enriched in (n-3) and (n-6) LCP from lipid peroxidation during the postnatal development of rats. The protection was more effectively in group C+E than in group B+E.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of radioanalytical and nuclear chemistry 192 (1995), S. 215-228 
    ISSN: 1588-2780
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Energy, Environment Protection, Nuclear Power Engineering
    Notes: Abstract Aerosol particles smaller than 1.8 μm were size-fractionated with micro-orifice impactors at two urban sites near Washington, DC, and analyzed for 44 elements including, As, Se, Sb, and Zn, i.e., elements strongly associated with coal combustion, incineration, and regionally transported secondary aerosol, by Instrumental Neutron Activation. Size distribution parameters were determined nonparametrically and with a least-squares peak-fitting method using impactor calibration data. Geometric and fitted mass mean aerodynamic diameters typically differed by 〈10% and increased continuously with increasing relative humidity (RH) in the range 56 to 79%, but along different curves for samples influenced by local and distant sources. The geometric mass mean diameters for samples influenced by winds from the direction of local sources were uniformly smaller than those influenced by westerly winds bearing aerosol from distant, regional, sources. At 60% RH, gmmads were As, 0.30±0.03 and 0.46±0.04; Se, 0.33±0.06 and 0.54±0.04; Sb, 0.39±0.03 and 0.53±0.04; and Zn, 0.39±0.06 and 0.53±0.08; respectively.
    Type of Medium: Electronic Resource
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