103 research outputs found
4680. Extraits des comptes et dépenses du roi Louis XI, dans M.-L. Cimber et F. Danjou, Archives curieuses de l'histoire de France, I, 91-109
No full text4680. Extraits des comptes et dépenses du roi Louis XI, dans M.-L. Cimber et F. Danjou, Archives curieuses de l'histoire de France, I, 91-109. In: Molinier Auguste. Les Sources de l'histoire de France - Des origines aux guerres d'Italie (1494). V. Introduction générale - Les Valois (suite), Louis XI et Charles VIII (1461-1494) Paris : A. Picard et fils, 1904. p. 31
4680. Extraits des comptes et dépenses du roi Louis XI, dans M.-L. Cimber et F. Danjou, Archives curieuses de l'histoire de France, I, 91-109
No full text4680. Extraits des comptes et dépenses du roi Louis XI, dans M.-L. Cimber et F. Danjou, Archives curieuses de l'histoire de France, I, 91-109. In: Molinier Auguste. Les Sources de l'histoire de France - Des origines aux guerres d'Italie (1494). V. Introduction générale - Les Valois (suite), Louis XI et Charles VIII (1461-1494) Paris : A. Picard et fils, 1904. p. 31
Impact of Gestational Diabetes mellitus (GDM) on Neonatal Outcome among Newborns Admitted to a Neonatal Intensive Care Unit
No full textIntroduction: Impact of GDM on neonatal outcome is unclear. Purpose: To determine the effect of maternal GDM on mortality and morbidity among newborns admitted to a neonatal intensive care unit (NICU). Methods: Historical cohort study. Exposed: Sixty-one newborns of women with GDM admitted to NICU (1998-2001). Controls: Sixty-one newborns of non-diabetic women. A matched (gestational age, gender, ethnicity, year of birth) pairs analysis (1:1) was performed. Main outcome measures: Congenital malformations, macrosomia, major neonatal morbidities and in-hospital mortality. Relative risks and 95% confidence limits were calculated for each variable. Results: No significant differences were observed for mortality (RR=1, p=0.683), incidence of congenital malformations (RR=0.4, p=0.131), macrosomia (RR=not calculable, 6.6% vs 0), perinatal asphyxia (RR=0.78, p=0.453), respiratory distress syndrome (RR=0.5, p=0.099), patent ductus arteriosus (RR=2.5, p=0.45), ischemic/hemorragic brain injury (RR=0.5, p=0.182), bronchopulmonary dysplasia (RR=2, p=0.683), and retinopathy of prematurity (RR=3, p=0.617). Conclusion: GDM did not influence significantly mortality and morbidity in our study population
De l'État et de l'avenir du chant ecclésiastique en France / par F. Danjou,...
No full textAvec mode text
La tuberculose nodulaire sous-cutanée des paupières / par le dr F. Danjou
No full textAvec mode texteOuvrages de référenc
GENOME-WIDE ASSOCIATION STUDY FOR HB F DETERMINANTS IN SARDINIAN PATIENTS WITH Β THALASSEMIA
No full textGenetic modifiers of β-thalassemia and clinical severity as assessed by age at first transfusion
No full textBackground The clinical and hematologic features of β-thalassemia are modulated by different factors, resulting in a wide range of clinical severity. The main factors are the type of disease-causing mutation and the ability to produce α-globin and γ-globin chains. In the present study we investigated the respective contributions of known modifiers to the prediction of the clinical severity of β-thalassemia as assessed by the patients' age at first transfusion. Design and Methods We studied the effect of seven loci in a cohort of 316 Sardinian patients with β0-thalassemia. In addition to characterizing the β-globin gene mutations, α-globin gene defects and HBG2:g.- 158C>T polymorphism, we genotyped two different markers in the BCL11A gene and three in the HBS1L-MYB intergenic region using single nucleotide polymorphism microarrays, imputation and direct genotyping. We performed Cox proportional hazard analysis of the time to first transfusion. Results According to the resulting model, we were able to explain phenotypic severity to a large extent (Harrell's concordance index=0.72; Cox & Snell R2=0.394) and demonstrated that most of the model's discriminatory ability is attributable to the genetic variants affecting fetal hemoglobin production (HBG2:g.-158C>T, BCL11A and HBS1L-MYB loci: C-index=0.68, R2=0.272), while the remaining is due to α-globin gene defects and gender. Consequently, significantly distinct survival curves can be described in our population. Conclusions This detailed analysis clarifies the impact of genetic modifiers on the clinical severity of the disease, measured by time to first transfusion, by determining their relative contributions in a homogeneous cohort of β0-thalassemia patients. It may also support clinical decisions regarding the beginning of transfusion therapy in patients with β-thalassemia. © 2012 Ferrata Storti Foundation
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