Plasma uridine as well as uric acid is elevated following fructose loading.
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Administration, Oral↗
Biomedical subjects
E M Allen
Publications and source records attributed to E M Allen.
A randomized, controlled study of the 1-hour and 24-hour effects of inhaled nitric oxide therapy in children with acute hypoxemic respiratory failure.
STUDY OBJECTIVE: To determine whether 24 h of inhaled nitric oxide improves oxygenation greater than conventional therapy alone in children with acute hypoxemic respiratory failure. DESIGN: Prospective, randomized, controlled study. SETTING: Twenty-six-bed pediatric ICU in a tertiary children's hospital. PATIENTS: Twenty-four patients with acute bilateral lung disease requiring a positive-end expiratory pressure >6 cm H2O and a fraction of inspired oxygen >0.5 for >12 h. INTERVENTIONS: Twelve patients were treated with 10 ppm inhaled nitric oxide from the onset of randomization and 12 control patients were initially maintained on a regimen of conventional therapy alone. After a period of 24 h, control patients were also treated with 10 ppm inhaled nitric oxide. Hemodynamic and blood gas measurements were performed at baseline, at 1 h after randomization, and at 24-h intervals for 2 days. MEASUREMENTS AND RESULTS: Inhaled nitric oxide decreased the ratio of pulmonary to systemic vascular resistance and improved oxygenation indexes during the initial hour following randomization. However, 24 h after randomization, the oxygenation indexes of 11 surviving treated patients were not improved in comparison to baseline or the oxygenation indexes of 10 surviving control patients. Oxygenation indexes acutely improved in control patients when inhaled nitric oxide was started after 24 h of conventional therapy. Oxygenation indexes remained improved in the initial control patients after 24 h of inhaled nitric oxide. CONCLUSIONS: Pulmonary vascular resistance and systemic oxygenation are acutely improved by 10 ppm inhaled nitric oxide in some children with severe lung disease. However, a sustained improvement in oxygenation may not occur during prolonged therapy. Thus, inhaled nitric oxide may have a limited therapeutic role in children with acute hypoxemic respiratory failure.
Acute Disease↗
The biobreeding Worcester rat--a model of organ-specific autoimmunity.
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Animals↗
Life events, social support and the risk of sudden infant death syndrome.
The effects of a lack of maternal social support and stressful life events on the risk of Sudden Infant Death Syndrome (SIDS) were examined by case-control design: 390 cases and 1592 control infants. A seven item index of mother's social support was used. A possible 21 life events experienced by each family were summed and then put into one of three categories: 0-2, 3-5, and 6 or more life events. Similar levels of maternal social support were found for both groups. SIDS families experienced significantly more stressful life events than control families, but once social factors had been taken into account this association was lost.
Analysis of Variance↗
The pathogenicity of spontaneously-occurring thyroglobulin-reactive T lymphocytes from BB/WOR rats.
Autoantigen-reactive T lymphocytes have been implicated in the pathogenesis organ-specific autoimmune disease. Thyroglobulin (Tg) is one of the primary autoantigens associated with autoimmune lymphocytic thyroiditis (LT). These experiments investigated the pathogenicity of a lymphocyte line derived from spontaneously-occurring Tg-reactive T lymphocytes isolated from unprimed NB line BB/Wor rats which have nearly a 100% incidence of spontaneous LT. Adoptive transfer of LT was accomplished by injecting 1.0 x 10(5) Tg-reactive lymphocytes into the tail vein of MHC compatible, non LT-prone BB line BB/Wor rats. All of the Tg-reactive cell line recipients (5/5) developed LT compared to only 20% (1/5) of the control rats given a parallel tetanus toxoid-reactive T cell line (p < 0.05, Fisher's exact test). Furthermore, despite the presence of LT, only one Tg-reactive cell line recipient developed insulitis. When Tg-reactive lymphocytes were incubated with an MHC compatible Wistar rat thyrocyte line at increasing effector: target ratios, the T cell line lysed thyrocytes in a dose-response fashion (r = 0.99, p < 0.05, linear regression), but did not lyse smooth muscle cell targets. FACS analysis established that this cell line is CD8 predominant. This is the first study to demonstrate that spontaneously-occurring Tg-reactive T lymphocytes from a nonimmunized animal model for LT are pathogenic. Further investigations into the repertoire of Tg-reactive lymphocytes in BB/Wor rats should provide insight into the pathogenesis of autoimmune thyroid disease and provide a basis for targeted immunotherapy.
Adoptive Transfer↗
A 36-year-old woman with altered sensorium.
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Adrenocorticotropic Hormone↗
HPLC micromethod for amrinone and metabolites in patients receiving concurrent cephalosporin therapy.
Amrinone (AMR), a bipyridine derivative, is receiving increasing use in postoperative cardiac patients as an inotrope and vasodilator. The hemodynamic response to amrinone in adults is linearly related to AMR concentrations, warranting therapeutic drug monitoring. We report a rapid microsample HPLC method for monitoring AMR and its principal metabolites, N-acetyl (N-ac) and N-glycolyl (N-gly) AMR. Serum was precipitated with acetonitrile, and the supernatant fluid was then injected into a C18 narrow-bore column. The mobile phase consisted of a 0.1 mol/L sodium phosphate buffer (pH 6) with a gradient of acetonitrile going from 50 to 100 mL/L of eluent. Detection with a diode-array detector (DAD) concurrently monitored the absorbances at 320 and 345 nm. Monitoring 320 nm allows optimal quantification of AMR, N-gly, and N-ac. Patients often receive concurrent cephalosporin therapy, which is detectable at 320 nm but not 345 nm. Because cephalosporins coelute with AMR or metabolites, monitoring at 345 nm allows separation of these antibiotics from AMR and metabolites while retaining a detection limit of 0.5 mg/L.
Acetonitriles↗
Hemodynamic effects of N-acetylamrinone in a porcine model of group B streptococcal sepsis.
High plasma concentrations of N-acetylamrinone, a primary metabolite of amrinone, are measured in some children during prolonged amrinone infusion. The purpose of this investigation was to determine if N-acetylamrinone has direct hemodynamic effects independent of amrinone. Twenty neonatal piglets received an infusion of 6 x 10(9) colony-forming units/kg of group B Streptococcus to induce sepsis. Subsequently, they were divided into 1 of 3 groups and received a 1-hr infusion of either normal saline (N = 4); 8 mg/kg amrinone, followed by 20 micrograms/kg/min (N = 9); or 8 mg/kg N-acetylamrinone, followed by 20 micrograms/kg/min (N = 7). Hemodynamic measurements and arterial/venous blood-gas determinations were obtained every 30 min during the study. Systemic vascular resistance and pulmonary vascular resistance were calculated. One milliliter of blood was obtained every 30 min during drug administration to determine plasma amrinone and N-acetylamrinone concentrations. The mean amrinone plasma concentrations measured at 30 and 60 min during the infusion time in the group receiving amrinone were 8.8 +/- 1.1 and 6.9 +/- 0.7 micrograms/ml, respectively. These animals experienced a significant decrease in mean pulmonary artery pressure and pulmonary vascular resistance, compared with saline controls after a 30-min infusion of amrinone. The mean N-acetylamrinone plasma concentrations measured at 30 and 60 min during the N-acetylamrinone infusion were 7.3 +/- 0.8 and 5.7 +/- 0.6 micrograms/ml, respectively. There was no difference between any hemodynamic parameter measured in these animals, compared with saline controls at any time during the infusion. We conclude that amrinone, but not N-acetylamrinone, causes pulmonary vasodilation in a porcine model of sepsis and that the parent drug is the sole active component in amrinone.
Amrinone↗
Oral dimercaptosuccinic acid and ongoing exposure to lead: effects on heme synthesis and lead distribution in a rat model.
Lead (Pb) exposure and subsequent toxicity continues to be a significant problem in the United States. Treatment with meso-2,3-dimercaptosuccinic acid (DMSA) has been reported to be effective in reducing the body's Pb burden, with fewer adverse side effects than other chelating agents. The oral availability and relative safety of DMSA presents the controversial option of treating patients with Pb poisoning on an outpatient basis. Despite recommendations that children be removed from the Pb contaminated environment, some children will inevitably be exposed to environmental Pb while receiving oral DMSA therapy. The study hypothesized that oral DMSA chelation therapy is beneficial even when faced with continued dietary Pb. Sprague-Dawley rats were exposed to Pb in water for 35 days and then placed in various treatment groups, including groups administered oral DMSA with and without concurrent Pb exposure. The concentration of Pb in blood and critical organs and Pb diuresis were measured. The effect of Pb on heme synthesis was determined by assaying the urinary delta-aminolevulinic acid (delta-ALA), and blood zinc protoporphyrin (ZPP). DMSA reversed the hematological effects of Pb, decreased the blood, brain, bone, kidney, and liver Pb concentration, and produced a marked Pb diuresis, even when challenged with ongoing Pb exposure. In conclusion, even though DMSA treatment without exposure to Pb is optimal, oral DMSA could be beneficial even when challenged with ongoing Pb exposure.
Administration, Oral↗
Thyroglobulin-reactive T lymphocytes in thyroiditis-prone BB/Wor rats.
Autoimmune lymphocytic thyroiditis (LT) is a common cause of primary hypothyroidism. Autoreactive T lymphocytes are clearly associated with this disorder, but their pathogenic role in spontaneously occurring LT remains to be established. In the present study, thyroglobulin-reactive T lymphocytes were cultured from young, unprimed LT-prone BB/Wor rats before the age of spontaneously-occurring LT. Although similar investigations have been conducted in animal models for experimental autoimmune thyroiditis (EAT), this study is unique because it examines a mammalian model for spontaneous LT. Splenic T lymphocytes were isolated from unprimed 30 to 45-day-old Fisher and LT-prone BB/Wor rats before the onset of LT, then tested for activation by normal (NL), iodine-poor (LI), and iodine-rich (HI) rat thyroglobulin (Tg) in bulk proliferation assay. BB/Wor rat lymphocytes were activated by all three Tg preparations, but Fisher lymphocytes were unresponsive (BB/Wor vs Fisher; p < 0.0001, Student's t-test). There was no difference between BB/Wor rat responses to the three preparations (p > 0.05, ANOVA). Based on these results, we conclude that Tg-responsive T lymphocytes can be cultured from young, unprimed LT-prone BB/Wor rats. Isolating such lymphocytes before the onset of histologically demonstrable LT strengthens the argument that antigen-specific T cells have a pathogenic role in the development of spontaneous autoimmune thyroid disease. The fact that these lymphocytes recognized normal, iodine-rich and iodine poor preparations of rat Tg equally well suggest that unlike the EAT model, spontaneously-occurring Tg-reactive T cells are not influenced by thyroglobulin's iodine content.
Animals↗
Antenatal and intrapartum factors associated with sudden infant death syndrome in the New Zealand Cot Death Study.
OBJECTIVE: To describe the relationship between antenatal and intrapartum factors and sudden infant death syndrome (SIDS). METHODOLOGY: The New Zealand Cot Death Study was a 3 year case-control study, with 485 infants who died from SIDS in the postneonatal period and 1800 randomly selected control infants. Data were obtained from obstetric records, parental interview and community nursing records. RESULTS: This study confirms many of the antenatal and intrapartum risk factors for SIDS noted in studies from both the southern and northern hemispheres. After controlling for potential confounders, such as occupational group and marital status, significant inverse effects were noted for interpregnancy interval, birthweight and gestation. Other factors that retained a significantly increased risk of SIDS were: increasing parity, bacteriological evidence of urinary tract infection (UTI) (adjusted odds ratio 1.73, 95% CI 1.10-2.73); smoking antenatally (AdjOR 2.14, 95% CI 1.61-2.84); less than six antenatal checks attended (AdjOR 1.84, 95% CI 1.19-2.84); second stage of labour less than 16 min (AdjOR 2.06, 95% CI 1.35-3.14) and multiple birth (AdjOR 3.23, 95% CI 1.70-6.02). No interaction was observed between maternal haemoglobin and antenatal smoking. Interactions were tested for and not found between antenatal smoking and three antenatal risk factors (UTI, short second stage of labour and number of antenatal appointments). The only significant interaction between these three factors and three modifiable postnatal risk factors (prone sleeping, bed sharing and bottle feeding) was between bed sharing and fewer antenatal appointments. The risk of SIDS associated with bed sharing was greater among those whose mothers had fewer antenatal appointments. CONCLUSIONS: Although many of the previously identified antenatal and intrapartum risk factors for SIDS are confirmed, the risks of SIDS associated with obstetric factors are in general considerably lower than the risks associated with the four modifiable postnatal risk factors.
Case-Control Studies↗
Difference between the measured and ordered dose of catecholamine infusions.
OBJECTIVE: To measure the actual concentrations of dopamine, dobutamine, and epinephrine in infusates prepared for patients, and to compare these concentrations with those of the dopamine HCl, dobutamine, and epinephrine HCl infusates that had been prescribed to evaluate drug preparation accuracy. DESIGN: Prospective, unblind study. SETTING: Pediatric intensive care unit in a tertiary-care teaching hospital. PARTICIPANTS: All dopamine, dobutamine, and epinephrine infusions ordered for patients during the 2-month study period were eligible for inclusion in the study. MEASUREMENTS: Daily samples of dopamine, dobutamine, and epinephrine infusates that were prepared for 41 pediatric patients were obtained; the infusate catecholamine concentration was measured by HPLC and compared with the ordered concentration. The concentration than was multiplied by the rate of infusion to determine the catecholamine dose. MAIN RESULTS: There were significant differences between the measured doses of dopamine, dobutamine, and epinephrine and the dopamine HCl, dobutamine, and epinephrine HCl doses (p = 0.0001, p = 0.039, and p = 0.0009, respectively) that had been ordered because of preparation inaccuracies. Failure to account for the HCl salt in the stock drug accounted for some, but not all, of the inaccuracy of the dopamine HCl and epinephrine HCl infusates. There was a wide interday variability in the measured catecholamine dosage in patients receiving the same dose for 3 days or more. CONCLUSIONS: There are daily fluctuations in the preparation of dopamine, dobutamine, and epinephrine infusates that could alter the amount of drug actually delivered to critically ill patients and potentially contribute to their hemodynamic instability.
Adolescent↗
Lithium sustains the acute antidepressant effects of sleep deprivation: preliminary findings from a controlled study.
Early morning sleep deprivation (patient awake from 0200 to 2200 hours) produces a same-day antidepressant effect in approximately one-half of patients with major depression. Unfortunately, these antidepressant effects are short-lived and patients usually relapse to baseline depression levels within 48 hours. Recent work suggests, however, that the use of lithium with early morning sleep deprivation sustains this rapid antidepressant effect and makes it clinically useful. In a 30-day study, we compared the abilities of four different treatments (lithium plus early morning sleep deprivation, lithium plus a control sleep deprivation procedure, and desipramine with either of the two sleep manipulations) to induce a rapid (next-day) and sustained antidepressant response in 16 depressed patients. Lithium plus early morning sleep deprivation produced a quicker response than lithium with the control sleep deprivation, and the response was sustained for at least 30 days. In this design, however, lithium/early morning sleep deprivation was no faster than either of the two desipramine/sleep deprivation conditions in inducing remission. These results support the results of previous studies and suggest further investigation of this novel sleep/pharmacologic intervention is warranted.
Adult↗
Factors adversely associated with breast feeding in New Zealand.
Control data from 1529 infants studied in a multicentre case-control study of sudden infant death in New Zealand were analysed to identify factors that might hinder the establishment and duration of breast feeding. Although 1300 infants (85%) were exclusively breast-fed at discharge from the obstetric hospital, this fell to 940 (61%) by 4 weeks. Logistic regression was used to identify factors that might adversely influence breast feeding 'at discharge', 'at 4 weeks' and the overall 'duration' of breast feeding. When adjusted for confounding factors, not exclusive breast feeding 'at discharge' was significantly associated with: twin pregnancy, being a Pacific Islander, mother not bedsharing, subsequent dummy use, birthweight less than 2500 g, heavy maternal smoking, not attending antenatal classes and mother less than 20 years old at first pregnancy. Mothers smoking more than 20 cigarettes a day were nearly twice as likely to not exclusively breast feed on discharge compared to those who did not smoke. A 'dose response' was apparent with the heaviest smokers having the least likelihood of establishing exclusive breast feeding. Being exclusively breast-fed at discharge but not 'at 4 weeks' was associated with: twin pregnancy, admission to a neonatal intensive care unit, subsequent dummy use and not being married. A shorter overall 'duration' of breast feeding was associated with maternal smoking, subsequent dummy use, mother not bedsharing, twin pregnancy, mother less than 20 years old at first pregnancy, low occupational status and not attending antenatal classes. These effects persisted when social and demographic factors, including birthweight, were taken into account.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Bed sharing, smoking, and alcohol in the sudden infant death syndrome. New Zealand Cot Death Study Group.
OBJECTIVES: To investigate why sharing the bed with an infant is a not consistent risk factor for the sudden infant death syndrome in ethnic subgroups in New Zealand and to see if the risk of sudden infant death associated with this practice is related to other factors, particularly maternal smoking and alcohol consumption. DESIGN: Nationwide case-control study. SETTING: Region of New Zealand with 78% of all births during 1987-90. SUBJECTS: Home interviews were completed with parents of 393 (81.0% of total) infants who died from the sudden infant death syndrome in the postneonatal age group, and 1592 (88.4% of total) controls who were a representative sample of all hospital births in the study region. RESULTS: Maternal smoking interacted with infant bed sharing on the risk of sudden infant death. Compared with infants not exposed to either risk factor, the relative risk for infants of mothers who smoked was 3.94 (95% confidence interval 2.47 to 6.27) for bed sharing in the last two weeks and 4.55 (2.63 to 7.88) for bed sharing in the last sleep, after other confounders were controlled for. The results for infants of non-smoking mothers were inconsistent with the relative risk being significantly increased for usual bed sharing in the last two weeks (1.73; 1.11 to 2.70) but not for bed sharing in the last sleep (0.98; 0.44 to 2.18). Neither maternal alcohol consumption nor the thermal resistance of the infant's clothing and bedding interacted with bed sharing to increase the risk of sudden infant death, and alcohol was not a risk factor by itself. CONCLUSION: Infant bed sharing is associated with a significantly raised risk of the sudden infant death syndrome, particularly among infants of mothers who smoke. The interaction between maternal smoking and bed sharing suggests that a mechanism involving passive smoking, rather than the previously proposed mechanisms of overlaying and hyperthermia, increases the risk of sudden infant death from bed sharing.
Adult↗
Ethnic differences in mortality from sudden infant death syndrome in New Zealand.
OBJECTIVES: To examine the factors which might explain the higher mortality from sudden infant death syndrome in Maori infants (7.4/1000 live births in 1986 compared with 3.6 in non-Maori children). DESIGN: A large nationwide case control study. SETTING: New Zealand. 485 infants who died of sudden infant death syndrome were compared with 1800 control infants. There were 229 Maori and 240 non-Maori cases of sudden infant death syndrome (16 cases unassigned) and 353 Maori and 1410 non-Maori controls (37 unassigned). RESULTS: Maori infants had 3.81 times the risk (95% confidence interval 3.06 to 4.76) of sudden infant death syndrome compared with non-Maori infants. The risk factors for sudden infant death syndrome within groups were remarkably similar. When Maori and non-Maori controls were compared the prevalence of many of the known risk factors was higher in Maori infants. In particular, mothers were socioeconomically disadvantaged, younger, and more likely to smoke and their infants were of lower birth weight and more likely to share a bed with another person. Multivariate analysis controlling for potential confounders found that simply being Maori increased the risk of sudden infant death syndrome by only 1.37 (95% CI = 0.95 to 2.01), not statistically significantly different from 1. Population attributable risk was calculated for prone sleeping position, maternal smoking, not breast feeding, and infants sharing a bed with another person. In total these four risk factors accounted for 89% of deaths from sudden infant death syndrome in Maori infants and 79% in non-Maori infants. CONCLUSION: The high rate of sudden infant death syndrome among Maori infants is based largely on the high prevalence in the Maori population of the major risk factors. Other risk factors, not related to ethnicity, probably explain remaining differences between Maori and non-Maori children.
Birth Weight↗
Pilot study of computerised differentiation of Huntington's disease, schizophrenic, and Parkinson's disease patients using the contingent negative variation.
In this study a potential known as the contingent negative variation was used to differentiate between schizophrenic, Parkinson's disease (PD), Huntington's disease (HD) patients and normal control subjects. The aim was to assist diagnosis and the avoidance of false diagnosis. 20 schizophrenic, 16 PD, 11 HD and 43 normal control subjects were enrolled for this study. The discriminatory variables were generated by applying spectral analysis to pre- and post-stimulus sections of the CNV responses. The patient differentiation was achieved by using the measured variables in a discriminant analysis program. It was possible to accurately differentiate between HD, schizophrenic, PD patients and normal control subjects. It was also attempted to differentiate between HD and schizophrenic patients, HD and PD patients, and schizophrenic and PD patients. The test results indicated that the method is useful in differentiating between these patients. This study had a number of limitations. It was based on a limited number of individuals, and an analysis of medication effects on the test results and the test-retest reliability assessment could not be carried out.
Diagnosis, Computer-Assisted↗
Acute iodine ingestion increases intrathyroidal glutathione.
In genetically predisposed individuals, autoimmune lymphocytic thyroiditis (LT) is potentiated by excess dietary iodine (I). There have been data which suggest that oxidative stress may have a role in iodine-induced LT. These in vivo studies were undertaken to examine the effect of iodine on intrathyroidal levels of the potent antioxidant glutathione (GSH) and see if the thyroids of LT-prone BB/Wor rats have aberrant GSH responses after iodine-loading. LT-prone BB/Wor, non LT-prone BB/Wor and Wistar rats were randomized to receive either 0.05% I (as Nal) or tap water. Thyroid and liver homogenates were assayed individually for GSH. Following the administration of 0.05% iodine water overnight, all of the animals demonstrated a rise in intrathyroidal GSH regardless of LT-proneness. To determine whether this was a dose-dependent response, Wis rats were randomized to receive tap, 0.0125%, 0.025%, 0.05%, or 0.075% I, overnight. Intrathyroidal GSH levels rose with increasing iodine concentrations peaking at 0.025% I. Hepatic GSH levels were unaltered by iodine treatment. Ten days of 0.05% I water did not result in any difference between the GSH levels of thyroids from treated and control rats. Frozen sections of the thyroids and livers from iodine-treated rats were compared to tap-water controls after staining with Mercury Orange for GSH and Schiff's reagent for evidence of lipid peroxidation. Iodine-treated thyroids had an apparent shift of GSH staining from the apical border to the cytoplasm. However, there was no Schiff's staining indicative of lipid peroxidation in the iodine-treated thyroids.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗