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A Brazilian Bacillus thuringiensis subspecies israelensis, toxic to Diptera, including mosquitoes, was found also to show toxicity to the coleopteran boll weevil Anthonomus grandis Boheman at an equivalent level to that of the standard coleopteran-active B. thuringiensis subspecies tenebrionis T08017. Recombinant B. thuringiensis strains expressing the individual Cyt1Aa, Cry4Aa, Cry4Ba and Cry11Aa toxins from this strain were assessed to evaluate their potential contribution to the activity against A. grandis, either alone or in combination. Whilst individual toxins produced mortality, none was sufficiently potent to allow calculation of LC50 values. Combinations of toxins were unable to attain the same potency as the parental B. thuringiensis subsp. israelensis, suggesting a major role for other factors produced by this strain.

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Angiotensin II (Ang II) is a multifunctional hormone that influences the function of cardiovascular cells through a complex series of intracellular signaling events initiated by the interaction of Ang II with AT1 and AT2 receptors. AT1 receptor activation leads to cell growth, vascular contraction, inflammatory responses and salt and water retention, whereas AT2 receptors induce apoptosis, vasodilation and natriuresis. These effects are mediated via complex, interacting signaling pathways involving stimulation of PLC and Ca2+ mobilization; activation of PLD, PLA2, PKC, MAP kinases and NAD(P)H oxidase, and stimulation of gene transcription. In addition, Ang II activates many intracellular tyrosine kinases that play a role in growth signaling and inflammation, such as Src, Pyk2, p130Cas, FAK and JAK/STAT. These events may be direct or indirect via transactivation of tyrosine kinase receptors, including PDGFR, EGFR and IGFR. Ang II induces a multitude of actions in various tissues, and the signaling events following occupancy and activation of Ang receptors are tightly controlled and extremely complex. Alterations of these highly regulated signaling pathways may be pivotal in structural and functional abnormalities that underlie pathological processes in cardiovascular diseases such as cardiac hypertrophy, hypertension and atherosclerosis.

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Angiotensin II (Ang II)* is a multifunctional hormone that influences the function of cardiovascular cells through a complex series of intracellular signaling events initiated by the interaction of Ang II with AT1 and AT2 receptors. AT1 receptor activation leads to cell growth, vascular contraction, inflammatory responses and salt and water retention, whereas AT2 receptors induce apoptosis, vasodilation and natriuresis. These effects are mediated via complex, interacting signaling pathways involving stimulation of PLC and Ca2+ mobilization; activation of PLD, PLA2, PKC, MAP kinases and NAD(P)H oxidase, and stimulation of gene transcription. In addition, Ang II activates many intracellular tyrosine kinases that play a role in growth signaling and inflammation, such as Src, Pyk2, p130Cas, FAK and JAK/STAT. These events may be direct or indirect via transactivation of tyrosine kinase receptors, including PDGFR, EGFR and IGFR. Ang II induces a multitude of actions in various tissues, and the signaling events following occupancy and activation of Ang receptors are tightly controlled and extremely complex. Alterations of these highly regulated signaling pathways may be pivotal in structural and functional abnormalities that underlie pathological processes in cardiovascular diseases such as cardiac hypertrophy, hypertension and atherosclerosis

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Longitudinal changes in physical activity among 129 Mexican-American (mean age 30.8; SD = 5.6) and 97 European-American (mean age 31.2; SD = 5.4) women were studied. Two physical activity recall interviews were administered at baseline and 7 years later. At baseline, European-American women reported more vigorous leisure activity (p < .005) than Mexican-Americans, and Mexican-Americans reported more moderate work activity (p < .02) than European-Americans. Virtually all components of physical activity increased significantly over the 7 years. Pearson tracking correlations for total energy expenditure were about r = 0.30. The finding that both groups increased physical activity overtime was unexpected and was unrelated to a reduction in the number of preschool children in the homes over time.

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Physical activity and dietary behaviors are often correlated in adults and adolescents. This association was examined in 351 Anglo- and Mexican-American children between the ages of 4 and 7 years. Behaviors were assessed by structured observations and interviews at home and school. Observed physical activity was significantly correlated with energy intake (r = .43), but was unrelated to the percentage of calories from total fat or saturated fat. Thus, interventions with young children to improve dietary behavior or physical activity should not be expected to automatically lead to changes in the other.

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OBJECTIVE: To assess the influence of several potential psychosocial determinants on children's eating behavior. PARTICIPANTS: Three hundred fifty-one Mexican-American and non-Hispanic white children (mean age = 4.4 years old at baseline) participated in the San Diego Study of Children's Activity and Nutrition for up to 2.5 years. METHODS: Child's eating behavior was described by 3 dependent variables: total energy, percentage energy from fat, and sodium intake per 1,000 kcal. Dietary information was collected 4 days a year using a 24-hour food intake record, which was a combination of direct observation and interviews with food preparers. The 35 predictor variables from child, parental, demographic, and environmental domains were collected by behavioral observation, interviewer-administered questionnaires, and physical measurements. STATISTICAL ANALYSES: Bivariate and regression analyses via mixed linear models were performed. RESULTS: Variables from the children's domain (such as skinfold thickness and weight) had the strongest associations with energy intake; parental variables (such as fat avoidance behavior and prompts to increase children's food intake) were associated with child's percentage energy from fat and sodium intake. In regression analyses, parsimonious subsets of variables accounted for 46% of variance in energy intake (3 variables), 40% of the variance in percentage of energy from fat (4 variables), and 44% of variance in sodium intake per 1,000 kcal energy (1 variable) in between-subject variance components. CONCLUSIONS: Fat and sodium intake of children may be improved by improving parents' nutrition habits and by having parents encourage children to eat a healthful diet. Few modifiable correlates of children's energy intake were identified.

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OBJECTIVE: To evaluate the relationship between insulin levels and cardiovascular risk factors in children and determine whether it varies among ethnic groups. METHODS: Cardiovascular risk factors and insulin levels were compared in 144 Mexican-American and Anglo-American mother-child pairs, when the children were 11 years of age. RESULTS: Although mean age did not differ between ethnicities, Mexican-American mothers and children both had a greater body mass index (mothers: 29.2 +/- 6.2 vs 27.2 +/- 7.9; children: 21.7 +/- 4.7 vs 19.7 +/- 4.6) and sum of skinfolds than did Anglo-Americans. Triglycerides, very low-density lipoprotein cholesterol, fasting insulin, and cholesterol/high-density lipoprotein ratio were higher, while high-density lipoprotein cholesterol was lower in both Mexican-American adults and children compared with Anglo-Americans. After adjusting for measures of obesity, only high-density lipoprotein cholesterol levels remained significantly lower in Mexican-Americans. For both adults and children, higher quartiles of insulin levels were associated with significantly higher triglycerides, blood pressure and lower high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol/apolipoprotein B levels (estimate of dense low-density lipoprotein size). A summary variable representing cardiovascular risk factors present in adult syndrome X patients was higher in both Mexican-American adults and children than in Anglo-Americans. CONCLUSION: Mexican-American children and adults have higher levels of many cardiovascular risk factors, and this appears related to higher insulin levels and overweight. Appropriate nutrition, weight control, and exercise at early ages could be important in slowing the development of atherosclerosis.

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Social interactions are important correlates of physical activity in children. Previous studies used global measures; the present study examined the influence of specific social interactions on immediate physical activity in children with data obtained from the Behaviors of Eating and Activity for Child Health: Evaluation System (BEACHES). The study examined parental and peer prompting of physical activity at home among 178 Mexican-American and 113 Anglo-American children at age 4 years and again at age 6.5 years. Most activity prompts came from adults interacting with children when they were sedentary. A reduction in the frequency of prompts from baseline to follow-up occurred in the prompter group (adult or child peer), gender, ethnicity, and preprompted activity level categories. Children's responses to these prompts showed that as they aged, they seemed to rely less on the interpersonal (especially adult) aspects of their environment for cues to be more active.

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Twenty-two potential correlates of children's physical activity were examined. Two hundred and one Mexican-American and 146 Anglo-American families with 4-year-old children were studied. Children's physical activity was directly observed in the evening at home on 4 visits for 1 hr each time. Anglo-American children and male children were found to be more active. Demographic variables explained 11% of the variance in children's physical activity. After adjusting for demographics, 3 children's variables and 6 social-family variables did not account for significantly more variance. Five environmental variables accounted for 11% additional variance. Variables observed concurrently with physical activity, such as time spent outdoors and prompts to be active, were highly associated with children's physical activity.

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A randomized, placebo-controlled trial of human surfactant given intratracheally at birth (prophylactic) versus rescue administration after the onset of severe respiratory distress syndrome (RDS) was conducted among preterm infants born at 24 to 29 weeks of gestation. Singleton fetuses were randomly assigned to receive (1) placebo (air), (2) prophylactic surfactant treatment, or (3) rescue surfactant treatment; infants of multiple births received either (1) prophylactic or (2) rescue treatment. Of 282 potentially eligible fetuses, 246 infants received treatments at birth and 200 infants had RDS. Outcomes are presented both as an intention-to-treat analysis (including infants who met exclusion criteria at or after birth) and as a full treatment protocol analysis for those infants with RDS and likely to benefit from surfactant. Preterm infants (mean 1.0 kg birth weight, 27 to 28 weeks of gestational age) randomly assigned to receive prophylactic treatment received surfactant soon after birth; those assigned to receive rescue surfactant had instillation at a mean age of 220 minutes if the lecithin-sphingomyelin ratio was less than or equal to 2.0 and no phosphatidylglycerol was detected in either amniotic fluid or initial airway aspirate, oxygen requirements were a fraction of inspired oxygen of greater than 0.5, and mean airway pressure was greater than or equal to 7 cm H2O from 2 to 12 hours after birth. Up to four treatment doses (or air) were permitted within 48 hours; approximately 60% of surfactant-treated infants required two or more doses. Surfactant-treated infants had significantly less pulmonary interstitial emphysema than placebo-treated infants (p = 0.02), but there were no other significant differences in mortality rates or morbidity. Indexes of oxygenation and ventilation were improved in surfactant recipients during the first 24 hours. An intention-to-treat analysis found no significant differences between infants given placebo and surfactant-treated infants or between prophylactic- and rescue-treated infants; an improved total mortality rate (p = 0.002) was found among surfactant-treated infants in Helsinki but not in San Diego. Among infants with RDS, the total mortality rate was significantly improved (p = 0.004) with surfactant treatment but not the proportion alive and without bronchopulmonary dysplasia at 28 days (p = 0.052), or the proportion alive and without bronchopulmonary dysplasia at 38 weeks of postconceptional age (p = 0.18) to adjust for differences in prematurity. Deaths caused by RDS or bronchopulmonary dysplasia were significantly reduced among surfactant recipients (p = 0.0001). Neither among singletons nor among multiple-birth infants was there a selective advantage to prophylactic versus rescue treatment.(ABSTRACT TRUNCATED AT 400 WORDS)

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Passive transcatheter coronary arterial perfusion, i.e., autoperfusion, has been introduced for clinical use to ameliorate short episodes of myocardial ischemia during percutaneous transluminal coronary angioplasty. The primary goal of this study was to evaluate the cardioprotective effect of autoperfusion after prolonged coronary artery occlusion. Accordingly, in 24 anesthetized dogs, either the left anterior descending or left circumflex coronary artery was occluded for 6 hours. The dogs were randomized to a control group subjected to coronary artery occlusion alone (n = 13) or to a group treated with transcatheter autoperfusion (n = 11). The hypoperfused zone, i.e., risk area and infarct size, were measured by autoradiography and triphenyltetrazolium chloride staining, respectively. The hypoperfused zone was 30 +/- 2% and 29 +/- 2% in the control and treated (NS) groups, respectively. When infarct size was expressed as a percent of the hypoperfused zone, it was 84 +/- 5% in the control group and 25 +/- 9% in the group treated with transcatheter autoperfusion (p less than 0.001), showing a reduction of 70%. In addition, an in vitro study showed pressure-dependent flow during autoperfusion as reflected by close linear relationship between perfusion pressure and flow (Flow = 0.54 X Pressure + 16.16, r = 0.99, n = 16). These data suggest that although passive coronary arterial perfusion for 6 hours after coronary occlusion does not prevent myocardial necrosis, it markedly reduces myocardial infarction in the canine model.

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