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1.
Clin Pediatr (Phila) ; 53(9): 845-53, 2014 Aug.
Article in English | MEDLINE | ID: mdl-24899633

ABSTRACT

OBJECTIVE: To assess the association of insurance status on infant rehospitalization in a population-based setting. METHODS: In this longitudinal retrospective study, hospitalizations were tracked for 1 year after birth discharge for 203 031 infants born in hospitals during 2008 using data from the New York State Inpatient Database. Relative risk was estimated using multivariable negative binomial regression models. RESULTS: Rehospitalization occurred in 9010 infants (4.4%). Medicaid coverage and being uninsured were strong predictors of rehospitalizations after adjustment for birth weight and other factors. Medicaid also bears a disproportionate share of the economic burden. Normal birth weight infants have the lowest risk, but comprise the majority of costs. Jaundice and acute bronchiolitis were the leading causes of rehospitalization within 30 days and 1 year, respectively. DISCUSSION: Future research can explore the preventability of rehospitalizations, and evaluate novel strategies for discharge and postnatal care coordination especially for uninsured and Medicaid-enrolled infants.


Subject(s)
Insurance, Health/statistics & numerical data , Medicaid/statistics & numerical data , Patient Readmission/statistics & numerical data , Acute Disease , Bronchiolitis/epidemiology , Humans , Infant , Infant, Newborn , Insurance Coverage , Jaundice, Neonatal/epidemiology , Longitudinal Studies , Medically Uninsured , New York/epidemiology , Patient Readmission/economics , United States
2.
N Engl J Med ; 364(19): 1837-43, 2011 May 12.
Article in English | MEDLINE | ID: mdl-21561349

ABSTRACT

Globin-gene mutations are a rare but important cause of cyanosis. We identified a missense mutation in the fetal Gγ-globin gene (HBG2) in a father and daughter with transient neonatal cyanosis and anemia. This new mutation modifies the ligand-binding pocket of fetal hemoglobin by means of two mechanisms. First, the relatively large side chain of methionine decreases both the affinity of oxygen for binding to the mutant hemoglobin subunit and the rate at which it does so. Second, the mutant methionine is converted to aspartic acid post-translationally, probably through oxidative mechanisms. The presence of this polar amino acid in the heme pocket is predicted to enhance hemoglobin denaturation, causing anemia.


Subject(s)
Fetal Hemoglobin/genetics , Hemoglobins, Abnormal/genetics , Mutation, Missense , gamma-Globins/genetics , Anemia/genetics , Cyanosis/genetics , Female , Humans , Infant, Newborn , Male , Methemoglobin/biosynthesis , Oxygen/blood , Protein Conformation , Sequence Analysis, DNA
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