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Biomedical subjects

E Cavalcanti

Publications and source records attributed to E Cavalcanti.

7 recordsLinked to original sources
PubMed1995

Identification of apolipoproteins A-I and B using high resolution electrophoresis on supported cellulose acetate.

A simple modification of high resolution electrophoresis on supported cellulose acetate is described. This modification is made by adding the surfactant Tween 20 to the buffer and permits the identification of apolipoproteins A-I and B as well as the usually detected serum proteins. The procedure is reproducible using various supported cellulose acetate plates with manual and automated procedures. Furthermore, this improved high resolution electrophoresis allows the semiquantitative evaluation of these apolipoproteins both on freshly collected and on -20 degrees C stored serum samples.

Apolipoprotein A-I↗
PubMed1995

Increased frequency of the C4A*6 rare allele in rheumatic heart disease.

The aim of the present investigation was to determine whether the alleles of the MHC class III complement proteins BF, C2 and C4 (C4A and C4B) could be markers for RHD in the Brazilian population. Forty-nine patients with chronic RHD were studied. The controls included 65 healthy unrelated individuals, matched with the patients according to sex, age and ethnical background. BF, C2, C4A and C4B allotypes were determined by standard technologies including Western blots for C2 and C4 variants with monoclonal and policlonal antibodies. The results showed a significantly elevated presence of the C4A*6 rare allele (p = 0.003 RR = 11.85) and a decrease of C4A*3 in the patients. In addition, C4 null and BF and C4 rare alleles were more frequent in patients than in the controls. Considering that in this investigation only RHD patients were included, further studies are necessary in order to clarify whether C4A6 is a marker for the cardiac form or for the disease itself.

Adolescent↗
PubMed1989

Insulin and glucagon degradation in liver are not affected by hepatic cirrhosis.

Hyperinsulinemia and impaired glucose tolerance are associated with liver cirrhosis. To investigate whether insulin-degrading activity in liver tissue plays a role in hyperinsulinemia, we assayed this activity in biopsy tissue from healthy and cirrhotic subjects. There was no difference in insulin degradation between these two groups. Also glucagon-degrading activity in liver tissue, which is catalyzed by the same enzyme as insulin-degrading activity, did not differ between the two groups studied. Therefore, insulin-degrading activity does not appear to be involved in the hyperinsulinemia that occurs in liver cirrhosis. The study provides indirect evidence that hyperinsulinemia and impaired glucose metabolism in liver cirrhosis are due to different mechanisms (receptorial and post-receptorial defects, and altered feedback inhibition of insulin secretion).

Adult↗