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G Kaltenborn

Publications and source records attributed to G Kaltenborn.

7 recordsLinked to original sources
PubMed1999

Quantification of lipids, liposomes, amino acids, and proteins by thermal ultramicrodigestion and an ultramicrocoulometric assay, based on the reaction of hypobromite with ammonia.

The quantification of nitrogen in organic material is described. It is based on a novel thermal ultramicrodigestion in combination with an ultramicrocoulometric quantification. The lower detection limit of the coulometric measurement is 0.5 microg nitrogen, which corresponds to 20 microg lipid, 3 microg glycine, or 4 microg protein. Therefore it is as sensitive as the frequently used Lowry method. In contrast to the Lowry protein determination it is not disturbed by detergents and most other interfering substances.

Amino Acids↗
PubMed1997

Simultaneous determination of fecal fat, nitrogen, and water by near-infrared reflectance spectroscopy.

BACKGROUND: Determinations of fecal fat and nitrogen reveal evidence of malabsorption and assist in estimating the efficacy of pancreatic enzyme treatment. Seventy-two-hour stool collection, with chemical analysis of fecal fat, and Kjeldahl's method for measurement of fecal nitrogen are generally accepted as standard methods for making these determinations. However, these traditional methods are expensive, time-consuming, and cumbersome. This study evaluated the efficiency and validity of an alternative method, using near-infrared reflectance spectroscopy (NIRS) and compared results with those of the standard methods. METHODS: Near-infrared reflectance spectroscopy is a secondary method: The instrument first has to be calibrated with samples analyzed by the standard method. Sixty-three stool samples with known fat content (range 4.79-292.5 mg/g), 24 samples with known nitrogen content (range 5.36-19.38 mg/g), and 24 samples with known water concentration (range 60.1-82.22%) served for calibration. A further 69 samples were analyzed to validate the procedure. RESULTS: There was a satisfactory correlation between the measurements produced by near-infrared reflectance spectroscopy and those produced by standard methods: fat r = 0.97; nitrogen r = 0.94; water r = 0.96. CONCLUSIONS: Near-infrared reflectance spectroscopy appears to be a reliable, simple, and rapid method of measuring different fecal components-as precise and accurate as the standard methods. Stool samples should be analyzed immediately after collecting or stored only a few days before analyzing.

Adolescent↗
PubMed1993

[Endogenous digitalis-like factor in liver cirrhosis and cholestasis].

Endogenous digitalis-like factor (EDLF), an inhibitor of membrane Na+/K(+)-ATPase, is discussed to be involved in the pathogenesis of cirrhogenic portal hypertension, ascites formation and development of functional hepatorenal failure. Therefore, we investigated the serum content of this mediator in patients with liver cirrhosis Child-Pugh stage A, B, and C (n = 27) by means of enzyme immunoassay with a specific digoxin antibody. Furthermore, a correlation analysis was performed in order to find out correlations between signs of cell injury, cholestasis, synthetic cell function, ascites formation, and hepatorenal failure. Our results demonstrate that EDLF is significantly elevated in Child C cirrhosis (0.61 +/- 0.15 ng/ml) in comparison to Child A cirrhosis (0.013 +/- 0.2 ng/ml) and is also higher than in Child B cirrhosis (0.23 +/- 0.25 ng/ml). In patients without ascites EDLF (0.056 +/- 0.19 ng/ml) differs significantly from that of patients with non-complicated ascites (0.156 +/- 0.176 ng/ml) and from that of patients with therapy refractory ascites (0.66 +/- 0.17 ng/ml) or hepatorenal failure (1.56 ng/ml). There are no correlations between EDLF and renal function. Significant correlations were demonstrated for cholestasis (serum bilirubin), synthesis function (serum protein, Quick's value, cholinesterase, fibrinogen, albumin), and the degree of portasystemic encephalopathy (number connection test). We conclude that EDLF may act as a mediator in the process of progressive portal hypertension and its complications due to cirrhosis. This process of progression is caused by the inhibition of Na+/K(+)-ATPase, vasoconstriction, and endothelin secretion.

Adult↗