Maternal age specific risk rate estimates for Down syndrome among live births in whites and other races from Ohio and metropolitan Atlanta, 1970-1989.

Our primary objective was to estimate, by one year and five year intervals, maternal age specific risk rates for Down syndrome among whites and among other races from two different populations, metropolitan Atlanta and south west Ohio, using live birth and prenatally diagnosed cases ascertained during 1970-1989. The five year estimates were also calculated separately for each of the five four year periods during these 20 years. Additionally, we compared two different methods of estimating these risk rates by using a third population of whites, and compared two different statistical methods of smoothing the risk rates. The results indicate good agreement between the metropolitan Atlanta and south west Ohio estimates within races, but show a statistically significant difference between the two race categories. Because 86% of live births in the "other races" category in the combined population are to blacks, these data may be seen as the first estimates of maternal age specific risk rates for Down syndrome among blacks calculated by one year intervals. We found excellent agreement in the risk rate estimates among the five four year time periods, between the estimates obtained by using the two different methods of estimation, and between the estimates obtained using the two different methods of statistical smoothing. Our estimated risk rates for white women in their 20s strongly reinforce those from previous studies currently being used for genetic counselling purposes. While we did find somewhat higher rates for women under 20, and increasingly higher rates for those over 30 years of age, these differences are not substantial. Thus, this study in general supports the risk rates estimated from data collected mostly during the 1960s and 1970s.

Human infection with B virus following a needlestick injury.

A 26-year-old veterinary technician who became infected with B virus at the site of a needlestick injury is described. After the patient was treated with intravenous acyclovir, all cultures became negative for B virus and have remained so during treatment with oral acyclovir. The literature on infections due to B virus in humans is reviewed, and a detailed discussion of the various aspects of this simian herpesvirus is presented.

Clinical chemistry reference values in two breeds of swine and their changes during percutaneous exposure to soman.

Clinical chemistry reference values in blood from 48 nonfasting Chester White/Yorkshire and 48 Hanford Miniature swine were determined. Subsequently, 40 animals of each breed were restrained in a cloth sling and fasted for 24 hours while exposed percutaneously to pinacolyl methylphosphonofluoridate (soman). The range of dosages for the Hanford Miniature swine was 2.0 to 15.8 mg/kg, and for the Chester White/Yorkshire swine, the range was 4.0 to 25.0 mg/kg. Sham-exposed groups, consisting of 8 animals of each breed, were treated in an identical manner, except no anticholinesterase agent was administered. Samples of blood were drawn at 1, 7, 14, and 28 days after soman or sham exposure. In the sham-exposed groups, significant changes from the reference values were observed as a result of the 24-hour restraint. In both breeds, skeletal muscle enzyme activities were increased, plasma cholinesterase activity (ChEPL) was decreased, calcium concentration was decreased, and phosphorus concentration was increased. Percutaneous exposure to soman resulted in decreases of ChEPL and erythrocyte cholinesterase activities (ChERBC). The ChEPL recovered more quickly than the ChERBC in both breeds. Even in asymptomatic swine, the decrease of ChERBC was greater than 60% after 24 hours. In the swine of each breed given the largest dosage, hyperglycemia was apparent in blood samples taken at the onset of apnea, especially when the animal survived for greater than 2 hours. We conclude that both breeds of swine, on the basis of dispersion in clinical chemistry reference values, were equally suited for this type of dermatotoxicity study. The sling method of restraint, however, caused some undesirable changes in biochemical values.

The effect of glucagon on urine amylase in various animal species.

Glucagon effects on the kidney include increased water, creatinine, and amylase clearance. We have compared these effects in several laboratory animal species. Although every species responded to glucagon, 1 mg iv, by some alteration in renal function there were differences in the degree and direction of the changes. Glucagon caused an increase in amylase clearance in four of the six species studied and an increase in creatinine clearance in four. An increase in urine flow tended to occur in all species. An increased amylase clearance is a feature of acute pancreatitis, and raised glucagon levels have been found during attacks. It is possible that the two are causally related. In the experimental situation, timing of urine collections and species differences were found to be of critical importance in exploring this possibility.