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  • Remodeling, Animal models of human disease, Hypertrophy  (2)
  • genetics  (2)
  • high temperature  (2)
  • Springer  (4)
  • American Heart Association (AHA)  (2)
  • The American Association of Immunologists (AAI)
  • The American Physiological Society (APS)
Publikationsart
Verlag/Herausgeber
  • Springer  (4)
  • American Heart Association (AHA)  (2)
  • The American Association of Immunologists (AAI)
  • The American Physiological Society (APS)
Erscheinungszeitraum
  • 1
    ISSN: 1572-8927
    Schlagwort(e): Equilibrium constant ; enthalpy change ; entropy change ; heat capacity change ; flow calorimetry ; high temperature ; magnesium chloride ; calcium chloride ; hydrochloric acid ; ion association ; isocoulombic reaction
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Chemie und Pharmazie
    Notizen: Abstract The aqueous reactions, Mg2++Cl−=MgCl+, Ca2++Cl−=CaCl+, and H+ +Cl−=HCl(aq), were studied as a function of ionic strength at 250, 275, 300, and 325°C using a flow calorimetric technique. The logK, ΔH, ΔS and ΔCp values were determined from the fits of the calculated and experimental heast. The data were reduced assuming a known functionality of the activity coefficient. Hence, the logK, ΔH, ΔS and ΔCp values determined in this study are dependent on the activity coefficient model used. These thermodynamic values were compared with literature results. The logK values for the formation of MgCl+ agree reasonably well with those reported in the literature. The logK values for CaCl+ formation agree reasonably well with those reported in the literature at 300 and 325°C. At lower temperatures, the agreement is poorer. The logK values for the formation of HCl(aq) are generally lower than those reported in the literature. The logK, ΔH, ΔS and ΔCp values for all three ion association reactions are positive and increase with temperature over the temperature range studied. These values are the first determined calorimetrically for the formation of MgCl+ and CaCl+ in the temperature range 275–325°C.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    Journal of solution chemistry 21 (1992), S. 789-801 
    ISSN: 1572-8927
    Schlagwort(e): Equilibrium constant ; enthalpy change ; entropy change ; heat capacity change ; flow calorimetry ; high temperature ; nitric acid ; ion association ; isocoulombic reaction
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Chemie und Pharmazie
    Notizen: Abstract The aqueous reaction, HNO3(aq)=H++NO 3 − was studied as a function of ionic strength I at 250, 275, 300 and 319°C using a flow calorimeter and the equilibrium constant K and enthalpy change (ΔH) at I=0 were determined. Using these experimental values, equations describing logK, ΔH, the entropy change ΔS and the heat capacity change ΔC p of reaction at I=0 and temperatures from 250 to 319°C were derived. The increasing importance of ion association as temperature rises was discussed. The use of an equation containing identical numbers of positive and identical numbers of negative charges on both sides of the equal sign (isocoulombic reaction principle) was applied to the logK values reported here and to those determined by others. The resulting plot of logK for the isocoulombic reaction vs. 1/T was fairly linear which supports the postulate that the principle is a useful technique for the extrapolation of logK values from low to high temperatures.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
    ISSN: 1432-0428
    Schlagwort(e): Keywords Diabetes mellitus ; insulin resistance ; genetics ; linkage analysis.
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The expansion of trinucleotide repeats has been associated with late-onset neurodegenerative disorders. Although the genes harbouring the triplet expansions may be widely expressed, the pathological expression of these diseases is restricted to specific tissues. Non-insulin-dependent diabetes mellitus (NIDDM) shares several features with diseases resulting from such dynamic mutations including late-onset and specific but limited sites of tissue pathology – muscle, fat, liver and insulin-secreting pancreatic beta cells. In order to examine the contribution of genes containing polymorphic CAG/CTG repeats to the development of NIDDM, we screened an adult human skeletal muscle cDNA library for expressed sequences containing tandem repeats of CAG and/or CTG. Ten different loci with polymorphic CAG/CTG repeats were identified, of which seven had a heterozygosity greater than 0.20. There was no evidence for linkage between these seven loci and NIDDM in a group of affected Mexican-American sib pairs. Nor was there a significant difference in the distribution of alleles between Caucasian patients with NIDDM and normal healthy control subjects or evidence for repeat expansion in diabetic subjects. Thus, muscle genes with polymorphic CAG/CTG repeats do not appear to play a significant role in the development of NIDDM. [Diabetologia (1996) 39: 725–730]
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
    ISSN: 1432-0428
    Schlagwort(e): Diabetes mellitus ; insulin resistance ; genetics ; linkage analysis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The expansion of trinucleotide repeats has been associated with late-onset neurodegenerative disorders. Although the genes harbouring the triplet expansions may be widely expressed, the pathological expression of these diseases is restricted to specific tissues. Non-insulin-dependent diabetes mellitus (NIDDM) shares several features with diseases resulting from such dynamic mutations including late-onset and specific but limited sites of tissue pathology — muscle, fat, liver and insulin-secreting pancreatic beta cells. In order to examine the contribution of genes containing polymorphic CAG/CTG repeats to the development of NIDDM, we screened an adult human skeletal muscle cDNA library for expressed sequences containing tandem repeats of CAG and/or CTG. Ten different loci with polymorphic CAG/CTG repeats were identified, of which seven had a heterozygosity greater than 0.20. There was no evidence for linkage between these seven loci and NIDDM in a group of affected Mexican-American sib pairs. Nor was there a significant difference in the distribution of alleles between Caucasian patients with NIDDM and normal healthy control subjects or evidence for repeat expansion in diabetic subjects. Thus, muscle genes with polymorphic CAG/CTG repeats do not appear to play a significant role in the development of NIDDM.
    Materialart: Digitale Medien
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
    Publikationsdatum: 2013-04-18
    Beschreibung: Nebivolol is a selective β1-blocker with nitric oxide–enhancing effects. MicroRNAs are small noncoding RNA molecules that downregulate gene expression. We compared the effects of nebivolol and atenolol, a first generation β1-selective blocker, on left ventricular hypertrophy, fibrosis, and function and microRNA expression in a rodent model of hypertension. Dahl salt-sensitive rats received either low-salt chow (control) or AIN-76A high-salt (8% NaCl) diet and randomized to vehicle (high-salt), nebivolol (20 mg/kg per day), or atenolol (50 mg/kg per day) for 8 weeks. High-salt induced left ventricular hypertrophy and fibrosis and decreased the expression of miR-27a, -29a, and -133a. Nebovolol attenuated deterioration of left ventricular systolic function, remodeling, and fibrosis more than atenolol, despite similar effects on heart rate and blood pressure. Nebivolol, but not atenolol, prevented the decrease in miR-27a and -29a induced by high-salt. Nebivolol and atenolol equally attenuated the decrease in miR-133a. In vitro overexpression of miR-27a,-29a, and -133a inhibited cardiomyocyte hypertrophy and reduced collagen expression. Both miR-27a and -29a target Sp1, and miR-133a targets Cdc42. Pharmacological inhibition of Sp1 and Cdc42 decreased myocardial fibrosis and hypertrophy. Our data support a differential microRNAs expression profile in salt-induced hypertension. Nebivolol substantially attenuated cardiac remodeling, hypertrophy, and fibrosis more than atenolol. These effects are related to attenuation of the hypertension-induced decrease in miR-27a and -29a (with a subsequent decrease in Sp1 expression) and miR-133a (with a subsequent decrease in Cdc42).
    Schlagwort(e): Remodeling, Animal models of human disease, Hypertrophy
    Print ISSN: 0194-911X
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
    Publikationsdatum: 2014-06-12
    Beschreibung: Interferon regulatory factor 1 (IRF1), a critical member of the IRF family, was previously shown to be associated with the immune system and to be involved in apoptosis and tumor suppression. However, the role of IRF1 in pressure overload–induced cardiac remodeling has remained unclear. Using genetic approaches, we established a central role for the IRF1 transcription factor in the regulation of cardiac remodeling both in vivo and in vitro, and we determined the mechanism underlying this process. The expression level of IRF1 was remarkably altered in both failing human hearts and hypertrophic murine hearts. Transgenic mice with cardiac-specific IRF1 overexpression exacerbated aortic banding–induced cardiac hypertrophy, ventricular dilation, fibrosis, and dysfunction, whereas IRF1-deficient (knockout) mice exhibited a significant reduction in the hypertrophic response. Similar results were observed in a global IRF1-knockout rat model. Mechanistically, the prohypertrophic effects elicited by IRF1 in response to pathological stimuli were associated with the direct activation of inducible nitric oxide synthase (iNOS). Furthermore, we identified 1 IRF1-binding site in the promoter region of the iNOS gene, which was essential for its transcription. To examine the IRF1-iNOS axis in vivo, we generated IRF1-transgenic/iNOS-knockout mice. IRF1 exerted profoundly detrimental effects in these mice; however, these effects were nullified by iNOS ablation. These data suggest the IRF1–iNOS axis as a crucial regulator of cardiac remodeling and that IRF1 could be a potent therapeutic target for cardiac remodeling.
    Schlagwort(e): Remodeling, Animal models of human disease, Hypertrophy
    Print ISSN: 0194-911X
    Thema: Medizin
    Standort Signatur Einschränkungen Verfügbarkeit
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