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E Wisniewski

Publications and source records attributed to E Wisniewski.

5 recordsLinked to original sources
PubMed2004

Complex data produce better characters.

Two studies were conducted to explore the use of complex data in character description and hybrid identification. In order to determine if complex data allow the production of better characters, eight groups of plant systematists were given two classes of drawings of plant parts, and asked to divide them into character states (clusters) in two separate experiments. The first class of drawings consisted only of cotyledons. The second class consisted of triplets of drawings: a cotyledon, seedling leaf, and inflorescence bract. The triplets were used to simulate complex data such as might be garnered by looking at a plant. Each experiment resulted in four characters (groups of clusters), one for each group of systematists. Visual and statistical analysis of the data showed that the systematists were able to produce smaller, more precisely defined character states using the more complex drawings. The character states created with the complex drawings also were more consistent across systematists, and agreed more closely with an independent assessment of phylogeny. To investigate the utility of complex data in an applied task, four observers rated 250 hybrids of Dubautia ciliolata X arborea based on the overall form (Gestalt) of the plants, and took measurements of a number of features of the same plants. A composite score of the measurements was created using principal components analysis. The correlation between the scores on the first principal component and the Gestalt ratings was computed. The Gestalt ratings and PC scores were significantly correlated, demonstrating that assessments of overall similarity can be as useful as more conventional approaches in determining the hybrid status of plants.

Asteraceae↗
PubMed1995

Distribution of flux control among the enzymes of mitochondrial oxidative phosphorylation in calcium-activated saponin-skinned rat musculus soleus fibers.

Metabolic control analysis was applied to describe the control of mitochondrial oxidative phosphorylation in calcium (approximately 2 microM free calcium) activated saponin-skinned rat musculus soleus fibers oxidizing glutamate and malate. Under these circumstances approximately 80% of mitochondrial active-state respiration was reached due to the activation of ATP turnover by actomyosin ATPase. The flux control coefficients of H(+)-ATPase, adenine-nucleotide translocase, phosphate transporter, NADH:ubiquinone oxidoreductase and cytochrome-c oxidase were determined to be equal to 0.16 +/- 0.08 (n = 6), 0.34 +/- 0.12 (n = 5), 0.08 +/- 0.03 (n = 5), 0.01 +/- 0.006 (n = 4) and 0.09 +/- 0.03 (n = 3) using inhibitor titrations with the specific inhibitors oligomycin, carboxyatractyloside, mersalyl, rotenone and cyanide, respectively, and applying non-linear regression of the entire titration curve. The flux control coefficient of actomyosin ATPase was determined with vanadate to be equal to 0.50 +/- 0.09 (n = 6), measuring independently the vanadate-caused inhibition of fiber respiration and ATP-splitting activity. In contrast to results with isolated rat skeletal muscle mitochondria reconstituted with soluble F1-ATPase the decrease in phosphate concentration from 10 mM to 1 mM only slightly affected the distribution of flux control coefficients. This difference is caused by different kinetic properties of soluble F1-ATPase and actomyosin ATPase. Therefore, phosphate seems to be in skeletal muscle in vivo only a modest modulator of control of oxidative phosphorylation.

Adenosine Diphosphate↗
PubMed1993

Phosphate affects the distribution of flux control among the enzymes of oxidative phosphorylation in rat skeletal muscle mitochondria.

The flux control coefficients of adenine nucleotide translocase, the phosphate transporter, and H(+)-ATPase were determined in rat skeletal muscle mitochondria using glutamate plus malate as substrates and soluble F1-ATPase as load enzyme. It was observed that the flux control coefficients of adenine nucleotide translocase, H(+)-ATPase, and the load enzyme F1-ATPase, at comparable rates of respiration, strongly depend on the phosphate concentration in the incubation medium. So, the flux control exerted by adenine nucleotide translocase, in the intermediate states of mitochondrial respiration (approximately 120 nmol of O2/min/mg) at 10 mM phosphate, was found to be about 0.37. At a phosphate concentration of 1 mM and comparable rates of respiration the flux control coefficient of the translocase decreased to about 0.20. Under these conditions, a sharp increase in the controlling influence of H(+)-ATPase from 0.10 to 0.74 was detected. Furthermore, at this flux rate, the sum of flux control coefficients of adenine nucleotide translocase, H(+)-ATPase, phosphate transporter, and the load enzyme F1-ATPase was noted to be very close to unity. This indicates that under the conditions of intermediate state respiration, all of the other reactions have a negligible controlling influence on oxidative phosphorylation in skeletal muscle mitochondria.

Animals↗
PubMed1987

The role of an anti-idiotype antibody in regulating hapten (azobenzenearsonate)-specific granuloma formation.

Antibody regulation of hapten-specific granulomas was studied in mice in order to assess the relationship between an anti-idiotypic antibody and granuloma formation. An anti-idiotypic antibody was raised against the idiotype of an azobenzenearsonate (ABA)-specific antibody of A/J mice. The anti-idiotypic antibody was subcutaneously (s.c.) administered to syngeneic mice prior to challenge with ABA-coupled polyacrylamide beads injected into the intestinal wall. The results of such a challenge were assessed histologically for granuloma formation at 24-h intervals. Mice primed with anti-Id antibody and challenged with ABA-linked beads developed epithelioid granulomas at 72 and 96 hr post-challenge. Unprimed mice or mice primed with control antibodies did not develop granulomas when challenged with ABA-linked beads. Moreover, we found that priming with anti-Id antibody intravenously (i.v.) resulted in suppression of intestinal granuloma formation that was similar to that observed previously after priming mice i.v. with ABA-coupled spleen cells (Ginsburg et al., 1982). This study demonstrates the induction and suppression of hapten-specific granuloma formation in the intestine by an anti-Id antibody. The observations indicate a role for the idiotype-anti-idiotype interaction in regulation of hapten-specific granuloma formation, and may have implications for the manner in which the host reacts against self in the autoimmune inflammatory process.

Animals↗