A consecutive and prospective series comprising 949 newborn infants of diabetic mothers treated during pregnancy and delivery in the period 1966--1977 has been analysed. The malformation rate was 8.2%. As compared to infants of mothers (White classes B-F alone) controlled outside pregnancy elsewhere, the rate of malformations was significantly reduced (from 14.1 to 7.4%) in fants whose mothers attended two hospitals specializing in the treatment and ambulatory control of diabetics. For diabetics not controlled at a diabetic centre outside pregnancy the malformation rate was 9% in classes B + C and 19.4% in classes D + F, compared to 6.2 and 8.5%, respectively, for those who were controlled. The rates of malformation (total as well as severe alone) were significantly reduced in infants of White's classes D + F, and insignificantly reduced in classes B + C (in class A no comparison could be made). The findings indicate that poor diabetic control outside pregnancy is teratogenic, although the 'disastrous malformation factor' of diabetes appears not to be totally dependent on the degree of compensation of the disbetic metabolism, as measured by the variables usually applied.

Adolescent↗

PubMedDate not supplied

Antibody-combining sites. Extending the natural limits.

The antibody repertoire is very large with at least 10(9) different antibody specificities, yet there are currently only 800 variable-region sequences known and < 23 Fab structures deposited with the Brookhaven Protein Data Bank. To engineer the antibody-combining site rationally, we need to define the rules that govern antibody structure. To understand the process of antibody-antigen recognition, we need not only to predict complementary determining regions accurately, but to simulate accurately the interaction of antibody with antigen. We have made progress in the modeling of antibody-combining sites and in the simulation of antibody complex formation. The combination of these approaches will allow us to extend the natural limits of antibody-combining sites in a more rational manner.

Algorithms↗

PubMedDate not supplied

Pediatric multiplane transesophageal echocardiography in congenital heart disease: new possibilities with a miniaturized probe.

In recent years, transducers for multiplane Doppler echocardiography have demonstrated their superior imaging performance in adult patients. To date, the size of these probes has limited their use in pediatric patients. In this article, we report our initial experience with a recently developed miniaturized transducer with all conventional imaging and Doppler modalities. The study focused primarily on imaging performance by comparing standard biplane images with those obtained in oblique planes. The investigations were carried out intraoperatively or during interventional catheterization in patients with congenital heart disease. We observed no complications in a study population of 15 children (weight range of 5 to 63 kg and an age range of 96 days to 11 years). The probe was easy to handle and provided excellent images. Additional information was obtained in several cases and documentation of clinical findings was easier because an optimal image plane almost always could be displayed. We concluded that pediatric multiplane Doppler echocardiography has considerably improved investigative performance compared with the conventional monoplane or biplane studies normally available for this age group. In neonates, however, investigation with the multiplane technique is limited by the size of the patient.

Child↗

PubMedDate not supplied

Strategic planning for hospices: a case study.

Explore the source record for details and available documents.

Connecticut↗

PubMedDate not supplied

Thrombocytopenia in a retrovirally-induced murine erythroleukemia.

A variant strain of Rauscher leukemia virus (RLV-A) obtained from a transplantable murine monomyelocytic leukemia causes a disease characterized by frank anemia, wasting, hepatosplenomegaly and erythroblastosis. The involvement of platelets in this disease are reported here. The RLV-A induced a severe thrombocytopenia (25 percent of control level) at the terminal stage of disease. This thrombocytopenia was not associated with disseminated intravascular coagulopathy since the prothrombin times were always within normal limits. The partial thromboplastin time was elevated in the terminal stages of disease and was found to be associated with factor deficiencies, possibly owing to the presence of anti-factor antibodies, in the intrinsic coagulation pathway, especially factor VIII. Further, splenectomy did not abolish the thrombocytopenia, since splenectomized, virally infected animals also developed severe thrombocytopenia (29 percent of control levels). The ensuing splenomegaly during progression of disease was not the cause of the thrombocytopenia. A physiological response to the severe thrombocytopenia was the production of larger size platelets. At terminal stages of the disease, platelet volume increased to 4.2 mu 3 (normal is 3.0 mu 3). An increase in platelet volume was also observed in splenectomized, virally infected animals. Electron microscopy indicated that these circulating platelets contained c-type viral particles. Viral infection was associated with decreased life span of circulating platelets, as measured by 75Se-methionine at mid and terminal stages of the disease. Our results suggest that direct viral infection of platelets and/or megakaryocytes with subsequent cell lysis is a possible cause of the observed thrombocytopenia observed in RLVA-induced disease and may also occur in other retrovirally-induced diseases.

Animals↗