Mitral stenosis: implications for critical care obstetric nursing.

Pregnancy complicated by mitral stenosis poses a significant risk for maternal morbidity and mortality. The perinatal nurse is challenged to use obstetric and cardiac physiologic principles in planning and guiding care during the intrapartum period. Nursing assessments and interventions based on these principles promote positive outcomes.

Monoclonal antibody C3.1 is a platelet derived growth factor (PDGF) antagonist.

A monoclonal antibody C3.1 raised against NR6 cells and partially purified PDGF receptor blocked PDGF stimulated [3H] thymidine incorporation in Swiss mouse 3T3 cells and immunoprecipitated a 180 kDa phosphoprotein from NR6 cells. The phosphoprotein bound to a C3.1 sepharose 4B affinity matrix and could be specifically eluted with PDGF but not by EGF or basic FGF. These preliminary results suggests that the ability of C3.1 to inhibit PDGF stimulated mitogenesis may be due to its direct or allosteric interaction at the PDGF receptor binding site.

Human platelet-derived growth factor. Purification and resolution into two active protein fractions.

Human platelets secrete a factor that stimulates cultured human cells to initiate DNA synthesis and to divide. This human platelet-derived growth factor (PDGF) has been purified congruent to 100,000-fold into two equally active homogeneous fractions, PDGF I (Mr congruent to 31,000) and PDGF II (Mr congruent to 28,000). The amino acid compositions of each are similar, highly basic, and show 18 half-cystine residues. Both PDGF I and II are glycoproteins, but differ in their carbohydrate compositions. The data suggest that PDGF II may be a proteolytic cleavage product of PDGF I but do not rule out that the proteins may be separate but very similar gene products. Purified PDGF is active in stimulating DNA synthesis at 0.2 ng/ml.

Diminution of bone mass in childhood diabetes.

Photon absorption measurements of forearm bone density in 196 insulin-dependent patients, age 6--26 years, were compared with findings in 124 controls. Expected density, gm. Ca/cm.2 bone width (M/W), was calculated from regressions of M/W on ulnar length for white and black male and female controls. There were no significant correlations between M/W differences from expected and serum Ca, Mg, P, or alkaline phosphatase levels, estimated physical activity level, insulin dosage, or the presence of joint contracture. White females averaged 8.2 per cent (+/- 1 S.E.M.) loss of M/W, as against white male average loss of 4.7 per cent +/- 1 and black female loss of 2 per cent +/- 2 (p less than 0.001); the black male population was too small for separate analysis. M/W loss greater than 10 per cent was seen in 29 per cent of white males, 19 per cent of blacks, and 48 per cent of white females (p less than 0.02). When the groups were further divided into those with duration of diabetes less than or equal to five years and those with duration greater than five years, significant reduction in M/W average loss over time was seen with white females (10.6 per cent +/- 1.2 to 3.7 per cent+/- 1.5, p less than 0.0001). Expression of this defect in bone mineralization is controlled by race and sex acting independently of each other.