Inferring the origin of populations introduced from a genetically structured native range by approximate Bayesian computation: case study of the invasive ladybird Harmonia axyridis.

Correct identification of the source population of an invasive species is a prerequisite for testing hypotheses concerning the factors responsible for biological invasions. The native area of invasive species may be large, poorly known and/or genetically structured. Because the actual source population may not have been sampled, studies based on molecular markers may generate incorrect conclusions about the origin of introduced populations. In this study, we characterized the genetic structure of the invasive ladybird Harmonia axyridis in its native area using various population genetic statistics and methods. We found that native area of H. axyridis most probably consisted of two geographically distinct genetic clusters located in eastern and western Asia. We then performed approximate Bayesian computation (ABC) analyses on controlled simulated microsatellite data sets to evaluate (i) the risk of selecting incorrect introduction scenarios, including admixture between sources, when the populations of the native area are genetically structured and sampling is incomplete and (ii) the ability of ABC analysis to minimize such risks by explicitly including unsampled populations in the scenarios compared. Finally, we performed additional ABC analyses on real microsatellite data sets to retrace the origin of biocontrol and invasive populations of H. axyridis, taking into account the possibility that the structured native area may have been incompletely sampled. We found that the invasive population in eastern North America, which has served as the bridgehead for worldwide invasion by H. axyridis, was probably formed by an admixture between the eastern and western native clusters. This admixture may have facilitated adaptation of the bridgehead population.

Dexamethasone effects on the hospital course of infants with bronchopulmonary dysplasia who are dependent on artificial ventilation.

A randomized double-blind placebo-controlled trial was conducted to evaluate the effects of enterally administered dexamethasone on the hospital course of infants with bronchopulmonary dysplasia. A total of 23 infants with a birth weight less than 1500 g who were dependent on artificial ventilation 3 to 4 weeks of age received dexamethasone (n = 12) or saline placebo (n = 11). Dexamethasone (0.5 mg/kg per day) was given in tapering doses for 7 days followed by hydrocortisone (8 mg/kg per day) which was progressively reduced for a total of 17 days of therapy. Infants who received dexamethasone required less oxygen on days 8 and 17 (P less than .05) and were more likely to extubate 8 days after therapy than infants in the control group (respectively 8/12 vs 3/11 infants, P less than .05; P = .12 after Yates correction). The use of dexamethasone significantly shortened median duration of mechanical ventilation (4 vs 22 days, P less than .05) but had no effect on length of oxygen therapy, hospitalization, home oxygen therapy, occurrence and severity of retinopathy of prematurity, rate of growth, and mortality. No significant complications resulted from dexamethasone therapy. Measurements of plasma dexamethasone levels confirmed the absorption of drug from the gastrointestinal tract (23.7 ng/mL in dexamethasone vs 4.6 ng/mL in the control group, P less than .05). Dexamethasone administration resulted in short-term improvements in pulmonary function but did not ameliorate the hospital course of infants with bronchopulmonary dysplasia.

Effect of prophylactic phenobarbital on intraventricular hemorrhage in high-risk infants.

Forty-two premature infants less than 24 hours of age, with normal admission echoencephalograms, were randomly assigned to control or phenobarbital treatment groups. Infants in the treated group received two loading doses of 10 mg/kg of phenobarbital 12 hours apart, followed by a maintenance dose of 2.5 mg/kg every 12 hours for 6 days. Serial echoencephalograms were obtained in both groups. The groups were comparable with regard to birth weight, gestational age, and potential risk factors for subependymal-intraventricular hemorrhage. Ten infants (48%) in each group developed hemorrhage. The hemorrhages in the phenobarbital-treated group were significantly less severe than those in the control group. The phenobarbital-treated infants who bled, however, were also significantly larger and more mature than control infants who bled. The results of this study indicate no effect of phenobarbital on the incidence of subependymal-intraventricular hemorrhage, but a possible beneficial effect on the severity of hemorrhage.

Neonatal hyperviscosity: randomized study of effect of partial plasma exchange transfusion on long-term outcome.

The use of partial plasma exchange transfusion in newborns with polycythemia and hyperviscosity was evaluated. Ninety-three infants with polycythemia and hyperviscosity were randomly assigned to receive either partial plasma exchange transfusion or symptomatic treatment; the infants were matched with control infants without polycythemia. Neonatal course and outcome at 1 and 2 years were evaluated for each of the three groups. Polycythemic infants had more fine motor and speech problems at 1 year of age than did control infants. At 2 years of age, polycythemic infants had more gross motor delays, neurologic diagnoses, fine motor abnormalities, and speech delays than did the control infants. There was no significant difference at 1 year between the polycythemic infants who had received partial plasma exchange transfusion and those given only symptomatic care. At 2 years, the group receiving partial plasma exchange transfusion had fewer neurologic diagnoses and fine motor abnormalities.

Analysis of the effects of applying federal diagnosis-related grouping (DRG) guidelines to a population of high-risk newborn infants.

Length of stay data collected for high-risk newborn infants admitted to a tertiary care children's hospital neonatal unit over a 6-year period were compared with mean and outlier lengths of stay published in the Federal Register as part of a proposed system for prospective payment of hospital cost by diagnosis-related groupings (DRGs). We found that the classification system for newborns markedly underestimated the number of days required for the treatment of these infants. The use of the geometric mean instead of the arithmetic mean as the measure of central tendency was a significant contributor to the discrepancy, especially in those subgroups with bimodal frequency distributions of lengths of stay. Another contributor to the discrepancy was the lack of inborn patients in the children's hospital cohort. The system of prospective payments, as outlined, does not take into account several factors that have a strong influence on length of stay such as birth weight (which requires more than three divisions to serve as an effective predictor), surgery, outborn status, and ventilation. Implementation of the system described in the Federal Register would severely discourage tertiary care referral hospitals from providing neonatal intensive care.

Maternal administration of vitamin K does not improve the coagulation profile of preterm infants.

The effect of maternal administration of vitamin K1 on cord blood prothrombin time, activated partial thromboplastin time, activity of factors II, VII, and X, and antigen levels of factors II and X in infants less than 35 weeks' gestation was evaluated. Pregnant women in preterm labor were randomly assigned to receive 10 mg of vitamin K1 intramuscularly or no injection. If delivery did not occur in 4 days, the dose of vitamin K1 was repeated. Women who continued their pregnancy 4 days beyond the second dose received 20 mg of vitamin K1 orally daily until the end of the 34th week of gestation. The birth weights of infants ranged from 370 to 2550 g and gestational age ranged from 22 to 34 weeks. The prothrombin time, activated partial thromboplastin time, factors II, VII, and X activity, and factors II and X antigen levels were not statistically different in either group of infants. Intraventricular hemorrhage occurred in 25 of 51 control infants and 25 of 47 vitamin K-treated infants. More control infants had grade III intraventricular hemorrhage on day 1 (P = .032), but on day 3 and 14 of life, the severity of intraventricular hemorrhage was comparable in both groups. Infants in whom an intraventricular hemorrhage developed were significantly smaller, younger, and more critically ill than infants without intraventricular hemorrhage. Administration of vitamin K1 to pregnant women at less than 35 weeks' gestation does not improve the hemostatic defects nor does it reduce the incidence or severity of intraventricular hemorrhage in their infants.

Incidence, presenting features, risk factors and significance of late onset septicemia in very low birth weight infants. The National Institute of Child Health and Human Development Neonatal Research Network.

BACKGROUND: Septicemia is a major antecedent of morbidity and mortality in very low birth weight (501- to 1500-g) infants. Our purpose was to determine prospectively the incidence, clinical presentation, laboratory features, risk factors, morbidity and mortality associated with late onset septicemia in infants 501 to 1500 g. METHODS: Clinical data were prospectively collected for 2416 infants enrolled in a multicenter trial to determine the efficacy of intravenous immunoglobulin in preventing nosocomial infections. Septicemia was confirmed by positive blood culture in 395 symptomatic infants. Multivariate analyses of factors associated with septicemia were performed. RESULTS: Sixteen percent of VLBW infants developed septicemia at a median age of 17 days. Factors associated with septicemia by logistic regression included male gender, lower gestational age and birth weight and decreased baseline serum IgG concentrations. Increasing apnea (55%), feeding intolerance, abdominal distension or guaiac-positive stools (43%), increased respiratory support (29%), lethargy and hypotonia (23%) were the dominant presenting features of septicemia. An abnormal white blood cell count (46%), unexplained metabolic acidosis (11%) and hyperglycemia (10%) were the most common laboratory indicators. Septicemic infants, compared with nonsepticemic infants, had significantly increased mortality (21% vs. 9%), longer hospital stay (98 vs. 58 days) and more serious morbidity, including severe intraventricular hemorrhage, bronchopulmonary dysplasia and increased ventilator days (P < 0.001). CONCLUSIONS: Late onset septicemia is common in very low birth weight infants, and the rate is inversely proportional to gestational age and birth weight. Septicemia is more common in males and those with low initial serum IgG values. A set of clinical signs (apnea, bradycardia, etc.) and laboratory values (leukocytosis, immature white blood cells and neutropenia) increase the probability of late onset sepsis, but they have poor positive predictive value.

Breast-milk jaundice.

PIP: The inhibiting agent of UDP-glucuronyl transferase (UDPGT), inhibition of which is associated with breast milk jaundice syndrome in infants, was thought to be 3(alpha),20(beta)-pregnandiol. European researchers have begun in vitro investigations to discover the inhibiting substance, and all studies have confirmed it is a nonesterified fatty acid. The strong association between breast milk jaundice, elevated values of nonesterified fatty acids, and unstimulated lipase in UDPGT-inhibitory milk was confirmed by electrophoretic technique. The mechanisms responsible for production of prolonged unconjugated hyperbilirubeinemia in infants, however, is not understood. 2 theories have been offered: 1) that milk triglyceride digestion before the milk reaches the duodenum leads to early absorption of most of the liberated glycerol that might otherwise be used by intestinal epithelium to resynthesize triglycerides; or 2) inhibitory human milk may facilitate the enterohepatic recirculation of bilirubin (reabsorption of bilirubin from intestinal lumen). Breast-feeding per se does not result in an increased incidence of neonatal hyperbilirubinemia; it is rather those infants who receive insufficient amounts of breast milk who develop the condition.^ieng

Monitoring critically ill newborn infants with digital capillary blood samples: an alternative.

Capillary blood samples obtained from a warmed distal phalanx of the right hand were compared with either temporal or right radial arterial blood samples for PO2, PCO2, and pH in 33 critically ill newborn infants. The blood pressure and skin temperatures of each infant and the ambient oxygen concentration were recorded at the time the blood was sampled. Sixty-eight paired PO2 analyses yielded a regression line close to the line of identity. The mean difference between digital capillary and arterial PO2 was 11.3 +/- 1.4 mm Hg (r = 0.92). The results were similar for the paired PCO2 analyses (r = 0.84) and for the paired pH analyses (r = 0.94). The correlation between arterial PO2 and digital capillary PO2 deteriorated when the systolic blood pressure of the patient was below 35 mm Hg. There was no correlation between skin temperature and capillary-arterial PO2 differences. The frequency of retrolental fibroplasia leading to blindness was not different from that in nurseries that sample umbilical arterial blood routinely.

The displacement of bilirubin from albumin by furosemide.

Since furosemide, a sulfonamide diuretic, has been recommended for use in the newborn infant, a study was made of its effect on the bilirubin-binding capacity of albumin. Furosemide was compared to sulfisoxazole, a known displacer of bilirubin, by means of three methods. First, aliquots of whole blood from 20 icteric infants were diluted in phosphate buffer along with expected clinical concentrations of furosemide and sulfisoxazole. The red cells and globulins were then isolated and bilirubin concentrations were measured in these two fractions. The addition of Furosemide resulted in the displacement of bilirubin from albumin to red cells and globulins. Mole for mole, furosemide displaced bilirubin about as well as sulfisoxazole. Second, the hydroxybenzeneazobenzoic acid dye binding test of Porter and twaters was performed using the sera of eight jaundiced newborn infants. The mean dye binding capacity of the sera was significantly reduced with the addition of furosemide to a final concentration of 2 mug/ml. Third, the administration of furosemide (5 mg/kg) or sulfisoxazole (50 mg/kg) to adult Gunn rats resulted in a significant fall in mean serum bilirubin concentration compared to saline controls. Furosemide, like sulfisoxazole, is a potent displacer of bilirubin and should be used with caution in jaundiced infants.