D. Halloran - Academia.edu (original) (raw)
Papers by D. Halloran
REFERENCES: 1 E. Broderick, et al (2005) J Biomed Mater Res 72B:37-42.
Pediatric Research, 2006
ABSTRACT
Journal of the American Dietetic Association, 2011
Journal of Perinatology, 2012
Objective-Examine the effect of prepregnancy weight and maternal gestational weight gain on postt... more Objective-Examine the effect of prepregnancy weight and maternal gestational weight gain on postterm delivery rates.
Journal of Perinatology, 2009
Objective-Determine the baseline incidence of birth asphyxia in neonatal intensive care unit (NIC... more Objective-Determine the baseline incidence of birth asphyxia in neonatal intensive care unit (NICU) survivors in a developing country and the early neurodevelopmental outcomes of such infants.
Pediatrics, 2008
Our goal was to estimate the quarterly prevalence of and evaluate trends for chronic medication u... more Our goal was to estimate the quarterly prevalence of and evaluate trends for chronic medication use in children.
Clinical Pediatrics, 2010
Objective-To evaluate the prevalence of atypical antipsychotic use in privately insured children ... more Objective-To evaluate the prevalence of atypical antipsychotic use in privately insured children and the diagnoses associated with treatment.
BJOG: An International Journal of Obstetrics & Gynaecology, 2011
To estimate the risk of short-term complications in neonates born between 34 and 36 weeks of gest... more To estimate the risk of short-term complications in neonates born between 34 and 36 weeks of gestation. This is a retrospective cohort study. Deliveries in 2005 in the USA. Singleton live births between 34 and 40 weeks of gestation. Gestational age was subgrouped into 34, 35, 36 and 37-40 completed weeks of gestation. Statistical comparisons were performed using chi-square test and multivariable logistic regression models, with 37-40 weeks of gestation designated as referent. Perinatal morbidities, including 5-minute Apgar scores, hyaline membrane disease, neonatal sepsis/antibiotics use, and admission to the intensive care unit. In all, 175,112 neonates were born between 34 and 36 weeks in 2005. Compared with neonates born between 37 and 40 weeks, neonates born at 34 weeks had higher odds of 5-minute Apgar <7 (adjusted odds ratio [aOR] 5.51, 95% CI 5.16-5.88), hyaline membrane disease (aOR 10.2, 95% CI 9.44-10.9), mechanical ventilation use >6 hours (aOR 9.78, 95% CI 8.99-10.6) and antibiotic use (aOR 9.00, 95% CI 8.43-9.60). Neonates born at 35 weeks were similarly at risk of morbidity, with higher odds of 5-minute Apgar <7 (aOR 3.42, 95% CI 3.23-3.63), surfactant use (aOR 3.74, 95% CI 3.21-4.22), ventilation use >6 hours (aOR 5.53, 95% CI 5.11-5.99) and neonatal intensive-care unit admission (aOR 11.3, 95% CI 11.0-11.7). Neonates born at 36 weeks remain at higher risk of morbidity compared with deliveries at 37-40 weeks of gestation. Although the risk of undesirable neonatal outcomes decreases with increasing gestational age, the risk of neonatal complications in late preterm births remains higher compared with infants delivered at 37-40 weeks of gestation.
Archives of Pediatrics & Adolescent Medicine, 2009
To estimate the sensitivity and specificity of pure-tone audiometry hearing screening in the prim... more To estimate the sensitivity and specificity of pure-tone audiometry hearing screening in the primary care setting. Prospective cohort study. Eight academic and private pediatric practices. A subset of children from a convenience sample of 1061 children between 3 and 19 years of age were screened for hearing loss using pure-tone audiometry. Intervention Formal audiologic evaluations (gold standard) for those children referred by their primary care physician (28 children) and for a random sample of children not referred (102 children). Main Exposure Pure-tone audiometry screening. Audiologic evaluations. A total of 28 children were referred to an audiologist for formal hearing testing after pure-tone audiometry screening during a well-child visit, at which 25 children did not pass the initial screening and 3 could not complete the screening. Of the 25 children, only 7 were evaluated by an audiologist, for a follow-up rate of 25%. One child was diagnosed as having hearing loss. Formal audiologic assessment was also performed on a random sample of 102 children who were not referred to the audiologist. For the random sample, hearing loss was identified in 2 of 76 (3%) children who passed and 1 of 16 (6%) children who did not pass pure tone audiometry screening. The sensitivity and specificity of pure-tone audiometry were 50% and 78%, respectively. In light of the increasing burden on physicians to provide preventive care, this study calls into question the value of hearing screening using pure-tone audiometry during well-child visits given the lack of follow-up after referral and the poor sensitivity.
Annals of Epidemiology, 2006
The aim of the study is to (i) reexamine risk factors for sudden infant death syndrome (SIDS) and... more The aim of the study is to (i) reexamine risk factors for sudden infant death syndrome (SIDS) and (ii) describe the relationship between length of gestation and age at death from SIDS. To evaluate risk factors for SIDS, we used multivariable logistic regression and included maternal demographic characteristics, maternal health and behavioral factors, and infant characteristics, including fetal growth, using US national linked birth and death files from 1996 to 1998. We used multivariable linear regression with mean postnatal age of death as the outcome of interest, controlling for the factors listed (referent length of gestation, 40 to 41 weeks). The crude SIDS rate was 0.7 deaths/1000 live births (8199 deaths). Length of gestation was a strong risk factor for SIDS, with the adjusted odds ratio (OR) greatest at shorter gestations: 28 to 32 weeks (OR, 2.9; 95% confidence interval, 2.6-3.2). Infants with gestations of 22 to 27 and 28 to 32 weeks died at mean ages of 20.9 (SD = 0.8) and 15.3 (SD = 0.5) weeks, respectively (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; or = 0.002). Term infants (40 to 41 weeks) died of SIDS at an adjusted mean age of 14.5 (SD = 0.4) weeks. Preterm birth continues to be a strong risk factor for SIDS after controlling for fetal growth. With increasing gestational age, mean age of SIDS death decreases considerably, with the postnatal age of death of very preterm infants 6 weeks later than that of term infants.
Experimental Biology and Medicine, 2010
Alpha-1-antitrypsin (a1AT) deficiency is caused by homozygosity for the a1AT mutant Z gene and oc... more Alpha-1-antitrypsin (a1AT) deficiency is caused by homozygosity for the a1AT mutant Z gene and occurs in one in 2000 Americans. The Z mutation confers an abnormal conformation on the a1AT mutant Z protein, resulting in accumulation within the endoplasmic reticulum of hepatocytes and chronic liver injury. Autophagy is one of several proteolytic mechanisms activated to cope with this hepatocellular protein burden, and is likely important in disposal of the unique polymerized conformation of the a1AT mutant Z protein, which is thought to be especially injurious to the cell. Recent data indicate that rapamycin may more efficiently upregulate autophagy when given in weekly dose pulses, as compared with a daily regimen. Therefore, we evaluated the effect of rapamycin on PiZ mice, a well-characterized model which recapitulates human a1AT liver disease. Daily dosing had no effect on autophagy, on accumulation of a1AT mutant Z protein or on liver injury. Weekly dosing of rapamycin did increase autophagic activity, as shown by increased numbers of autophagic vacuoles. This was associated with reduction in the intrahepatic accumulation of a1AT mutant Z protein in the polymerized conformation. Markers of hepatocellular injury, including cleavage of caspase 12 and hepatic fibrosis, were also decreased. In conclusion, this is the first report of a successful in vivo method for reduction of intrahepatic a1AT mutant Z polymerized protein. Application of this finding may be therapeutic in patients with a1AT deficiency by reducing the intracellular burden of the polymerized, mutant Z protein and by reducing the progression of liver injury.
REFERENCES: 1 E. Broderick, et al (2005) J Biomed Mater Res 72B:37-42.
Pediatric Research, 2006
ABSTRACT
Journal of the American Dietetic Association, 2011
Journal of Perinatology, 2012
Objective-Examine the effect of prepregnancy weight and maternal gestational weight gain on postt... more Objective-Examine the effect of prepregnancy weight and maternal gestational weight gain on postterm delivery rates.
Journal of Perinatology, 2009
Objective-Determine the baseline incidence of birth asphyxia in neonatal intensive care unit (NIC... more Objective-Determine the baseline incidence of birth asphyxia in neonatal intensive care unit (NICU) survivors in a developing country and the early neurodevelopmental outcomes of such infants.
Pediatrics, 2008
Our goal was to estimate the quarterly prevalence of and evaluate trends for chronic medication u... more Our goal was to estimate the quarterly prevalence of and evaluate trends for chronic medication use in children.
Clinical Pediatrics, 2010
Objective-To evaluate the prevalence of atypical antipsychotic use in privately insured children ... more Objective-To evaluate the prevalence of atypical antipsychotic use in privately insured children and the diagnoses associated with treatment.
BJOG: An International Journal of Obstetrics & Gynaecology, 2011
To estimate the risk of short-term complications in neonates born between 34 and 36 weeks of gest... more To estimate the risk of short-term complications in neonates born between 34 and 36 weeks of gestation. This is a retrospective cohort study. Deliveries in 2005 in the USA. Singleton live births between 34 and 40 weeks of gestation. Gestational age was subgrouped into 34, 35, 36 and 37-40 completed weeks of gestation. Statistical comparisons were performed using chi-square test and multivariable logistic regression models, with 37-40 weeks of gestation designated as referent. Perinatal morbidities, including 5-minute Apgar scores, hyaline membrane disease, neonatal sepsis/antibiotics use, and admission to the intensive care unit. In all, 175,112 neonates were born between 34 and 36 weeks in 2005. Compared with neonates born between 37 and 40 weeks, neonates born at 34 weeks had higher odds of 5-minute Apgar <7 (adjusted odds ratio [aOR] 5.51, 95% CI 5.16-5.88), hyaline membrane disease (aOR 10.2, 95% CI 9.44-10.9), mechanical ventilation use >6 hours (aOR 9.78, 95% CI 8.99-10.6) and antibiotic use (aOR 9.00, 95% CI 8.43-9.60). Neonates born at 35 weeks were similarly at risk of morbidity, with higher odds of 5-minute Apgar <7 (aOR 3.42, 95% CI 3.23-3.63), surfactant use (aOR 3.74, 95% CI 3.21-4.22), ventilation use >6 hours (aOR 5.53, 95% CI 5.11-5.99) and neonatal intensive-care unit admission (aOR 11.3, 95% CI 11.0-11.7). Neonates born at 36 weeks remain at higher risk of morbidity compared with deliveries at 37-40 weeks of gestation. Although the risk of undesirable neonatal outcomes decreases with increasing gestational age, the risk of neonatal complications in late preterm births remains higher compared with infants delivered at 37-40 weeks of gestation.
Archives of Pediatrics & Adolescent Medicine, 2009
To estimate the sensitivity and specificity of pure-tone audiometry hearing screening in the prim... more To estimate the sensitivity and specificity of pure-tone audiometry hearing screening in the primary care setting. Prospective cohort study. Eight academic and private pediatric practices. A subset of children from a convenience sample of 1061 children between 3 and 19 years of age were screened for hearing loss using pure-tone audiometry. Intervention Formal audiologic evaluations (gold standard) for those children referred by their primary care physician (28 children) and for a random sample of children not referred (102 children). Main Exposure Pure-tone audiometry screening. Audiologic evaluations. A total of 28 children were referred to an audiologist for formal hearing testing after pure-tone audiometry screening during a well-child visit, at which 25 children did not pass the initial screening and 3 could not complete the screening. Of the 25 children, only 7 were evaluated by an audiologist, for a follow-up rate of 25%. One child was diagnosed as having hearing loss. Formal audiologic assessment was also performed on a random sample of 102 children who were not referred to the audiologist. For the random sample, hearing loss was identified in 2 of 76 (3%) children who passed and 1 of 16 (6%) children who did not pass pure tone audiometry screening. The sensitivity and specificity of pure-tone audiometry were 50% and 78%, respectively. In light of the increasing burden on physicians to provide preventive care, this study calls into question the value of hearing screening using pure-tone audiometry during well-child visits given the lack of follow-up after referral and the poor sensitivity.
Annals of Epidemiology, 2006
The aim of the study is to (i) reexamine risk factors for sudden infant death syndrome (SIDS) and... more The aim of the study is to (i) reexamine risk factors for sudden infant death syndrome (SIDS) and (ii) describe the relationship between length of gestation and age at death from SIDS. To evaluate risk factors for SIDS, we used multivariable logistic regression and included maternal demographic characteristics, maternal health and behavioral factors, and infant characteristics, including fetal growth, using US national linked birth and death files from 1996 to 1998. We used multivariable linear regression with mean postnatal age of death as the outcome of interest, controlling for the factors listed (referent length of gestation, 40 to 41 weeks). The crude SIDS rate was 0.7 deaths/1000 live births (8199 deaths). Length of gestation was a strong risk factor for SIDS, with the adjusted odds ratio (OR) greatest at shorter gestations: 28 to 32 weeks (OR, 2.9; 95% confidence interval, 2.6-3.2). Infants with gestations of 22 to 27 and 28 to 32 weeks died at mean ages of 20.9 (SD = 0.8) and 15.3 (SD = 0.5) weeks, respectively (p &amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;amp;lt; or = 0.002). Term infants (40 to 41 weeks) died of SIDS at an adjusted mean age of 14.5 (SD = 0.4) weeks. Preterm birth continues to be a strong risk factor for SIDS after controlling for fetal growth. With increasing gestational age, mean age of SIDS death decreases considerably, with the postnatal age of death of very preterm infants 6 weeks later than that of term infants.
Experimental Biology and Medicine, 2010
Alpha-1-antitrypsin (a1AT) deficiency is caused by homozygosity for the a1AT mutant Z gene and oc... more Alpha-1-antitrypsin (a1AT) deficiency is caused by homozygosity for the a1AT mutant Z gene and occurs in one in 2000 Americans. The Z mutation confers an abnormal conformation on the a1AT mutant Z protein, resulting in accumulation within the endoplasmic reticulum of hepatocytes and chronic liver injury. Autophagy is one of several proteolytic mechanisms activated to cope with this hepatocellular protein burden, and is likely important in disposal of the unique polymerized conformation of the a1AT mutant Z protein, which is thought to be especially injurious to the cell. Recent data indicate that rapamycin may more efficiently upregulate autophagy when given in weekly dose pulses, as compared with a daily regimen. Therefore, we evaluated the effect of rapamycin on PiZ mice, a well-characterized model which recapitulates human a1AT liver disease. Daily dosing had no effect on autophagy, on accumulation of a1AT mutant Z protein or on liver injury. Weekly dosing of rapamycin did increase autophagic activity, as shown by increased numbers of autophagic vacuoles. This was associated with reduction in the intrahepatic accumulation of a1AT mutant Z protein in the polymerized conformation. Markers of hepatocellular injury, including cleavage of caspase 12 and hepatic fibrosis, were also decreased. In conclusion, this is the first report of a successful in vivo method for reduction of intrahepatic a1AT mutant Z polymerized protein. Application of this finding may be therapeutic in patients with a1AT deficiency by reducing the intracellular burden of the polymerized, mutant Z protein and by reducing the progression of liver injury.