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Biomedical subjects

K Raivio

Publications and source records attributed to K Raivio.

15 recordsLinked to original sources
PubMed1992

N-terminal propeptide of type III collagen in tracheal fluid and serum in preterm infants at risk for bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD) is a common pulmonary complication in preterm infants that leads to fibrosis of the bronchoalveolar walls and often to severe clinical consequences. Type III collagen is deposited early in progressive fibrosis. Because the N-terminal propeptide of type III collagen (PIIINP), a by-product of type III collagen synthesis, reflects the degree of pulmonary fibrosis in adults, we hypothesized that PIIINP in tracheal aspirates and/or serum may be a useful early marker of developing BPD in neonates. We serially measured PIIINP in tracheal fluid and serum samples during the first weeks of life in 41 consecutive respirator-treated preterm infants (mean birth weight 1067 g, mean gestational age 28.3 wk). Eight of the infants died and 22 infants fulfilled the criteria for BPD at age 28 d. The mean level of PIIINP decreased with advancing postnatal age in tracheal fluid but not in serum. The mean tracheal fluid PIIINP during d 1 and 2 of life, respectively, was 175 and 200 ng/mg protein in infants who were still in a respirator at age 28 d (n = 13), 122 and 97 ng/mg protein in those who were weaned earlier (n = 20), and 50 and 30 ng/mg protein in those who died before age 28 d (n = 8). These differences are not statistically significant, and the variability of the values was large. The PIIINP concentrations in tracheal aspirates of infants subsequently developing BPD did not differ from those without BPD. Neither did the levels correlate with the degree of BPD or radiologically defined fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Biomarkers↗
PubMed1992

[Gene therapy].

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Clinical Trials as Topic↗
PubMed1977

Purine metabolism and control of cell proliferation.

Exposure of normal lymphocytes to phytohaemagglutinin or other lectin mitogens results in increased concentrations of 5-phosphoribosyl-1-pyrophosphate (PP-ribose-P) within minutes. Subsequently, synthesis of purine nucleotides by both the de novo and the salvage pathways is facilitated. This change is prevented by proliferation-inhibiting concentrations of exogenous adenosine. The capacity of lymphocytes to metabolize both adenine and adenosine is increased several-fold by incubation with phytohaemagglutinin but the specific activities of the respective first-step enzymes are not significantly altered. These results suggest that the relatively low quantity of PP-ribose-P available in normal lymphocytes is a major factor limiting the synthesis of purine nucleotides and may be important for the maintenance of the quiescent state. Increased availability of PP-ribose-P may also be associated with proliferative activation of fibroblast-like cells: chick embryo fibroblast cultures released from density-dependent inhibition of growth by insulin, trypsin or serum rapidly increase the rate of adenine incorporation into nucleotides. Chick embryo fibroblasts transformed by Rous sarcoma virus, but not cells infected with the respective non-transforming leukosis virus, show PP-ribose-P concentrations higher than those observed in normal cells.

Adenine↗
PubMed1976

Enzymatic diagnosis and carrier detection of aspartylglucosaminuria using blood samples.

The activity of the glycoprotein degrading lysosomal hydrolase, 4-L-aspartylglycosylamine amido hydrolase (AAD Gase, EC.3.5.1.26), was measured in plasma, buffy coat leukocytes, and separated lymphocytes (Ficoll separation) from 16 patients with aspartylglucosaminuria (AGU), 29 obligate heterozygotes, and 30 control subjects. In lymphocytes the AGU patients had unmeasurable or minimal AAD Gase activity with a mean of 3.9 U. The obligate heterozygotes showed AAD Gase activities ranging from 5 to 69 U with a mean of 34.1 U. Enzyme activities in the control group ranged from 91 to 243 U with a mean of 127.9 U, and were clearly separated from the values of the heterozygotes. In leukocytes the AGU patients had unmeasurable enzyme activity and obligate heterozygotes had enzyme levels closely similar to those in the lymphocytes from the same individuals. The AAD Gase activity in the leukocytes of the control group displayed a much wider variation than in the lymphocytes, ranging from 22 to 132 U with a mean of 70.7 U. In plasma the AGU patients had undetectable AAD Gase activity. The mean enzyme level of obligate heterozygotes was 72.2 U and that of control individuals 107.2 U, but the overlap between the groups was extensive. The results indicate that homozygous deficiency of AAD Gase, i.e., aspartylglucosaminuria can be reliably diagnosed using plasma, leukocytes, or separated lymphocytes. For carrier detection only separated lymphocytes allow a satisfactory differentiation between heterozygous and normal individuals. A group of 31 siblings of verified AGU cases and 11 children of identified carriers, whose spouses had normal AAD Gase activity, were investigated using the lymphocyte assay. The observed and expected frequencies (on the basis of Mendelian probabilities) were closely similar, suggesting that the lymphocyte assay can be used reliably for carrier detection.

Acetylglucosaminidase↗
PubMed1975

Prenatal diagnosis and fetal pathology of I-cell disease (mucolipidosis type II).

Increased activity of several lysosomal hydrolases was demonstrated in amniotic fluid from a fifteenth week pregnancy in which the fetus had I-cell disease. Cultured cells from amniotic fluid had a decreased activity of the same enzymes. The diagnosis of I-cell disease was later confirmed by enzyme assays in cell cultures of fetal skin and by morphologic studies of several tissues from the aborted fetus. Electron microscopic studies of the fetal tissues and cultured fibroblasts had large numbers of typical inclusions of I-cell disease, thus substantiating the diagnosis and intrauterine manifestation of the disease. The results indicate that prenatal diagnosis of I-cell disease is possible with enzyme assays of amniotic fluid and in cultures of fetal cells from the fluid. Enzyme studies of amniotic fluid can provide a preliminary diagnosis within a few hours, but it is suggested that the definitive diagnosis should be based on assays in cultured cells from amniotic fluid.

Acetylglucosaminidase↗
PubMed1975

[Hyperuricemia].

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Humans↗