Association of ABO and Rh incompatibility with neonatal hyperbilirubinaemia

Background: 60% of term new-born have clinical jaundice, in the first week of life. ABO incompatibility is the most common cause of haemolytic disease of the new-born. So early intervention, at proper time, is mandatory to prevent these sequelae.Methods: This study was done at Dhiraj Hospital in Obstetrics and Gynecology Department. It was prospective observational study. 200 new-born with ABO incompatibility and 20 new-born with Rh incompatibility, causing clinically significant neonatal hyperbilirubinemia, were recruited for the clinical study noted.Results: The incidence of ABO incompatibility in our study was 13.79% and of Rh incompatibility was 1.37%. In ABO incompatibility group, 90% new born developed clinical jaundice. In treated group, out of 88 new born, 82 were from O-A and O-B incompatibility group. In ABO incompatibility DCT was positive in only 9%, whereas in Rh incompatibility it was 25%. In ABO incompatibility group, majority, 56% did not require treatment, whereas in Rh incompatibility group 65% required treatment. In ABO incompatibility group only 1% required exchange transfusion whereas in Rh incompatibility, it was required in 10%. In ABO incompatibility, all new-born treated well except, 0.5% developed kernicterus. In Rh incompatibility group, 10% new-born developed kernicterusConclusions: In ABO incompatibility, if jaundice develops, it remains in physiological limits. In presence of some aggravating conditions may present as pathological jaundice. It results in significant morbidity but no mortality. So prevention of aggravating factors is very important, in case of ABO incompatibility.

Genomic Profiling of Childhood Tumor Patient-Derived Xenograft Models to Enable Rational Clinical Trial Design.

Accelerating cures for children with cancer remains an immediate challenge as a result of extensive oncogenic heterogeneity between and within histologies, distinct molecular mechanisms evolving between diagnosis and relapsed disease, and limited therapeutic options. To systematically prioritize and rationally test novel agents in preclinical murine models, researchers within the Pediatric Preclinical Testing Consortium are continuously developing patient-derived xenografts (PDXs)-many of which are refractory to current standard-of-care treatments-from high-risk childhood cancers. Here, we genomically characterize 261 PDX models from 37 unique pediatric cancers; demonstrate faithful recapitulation of histologies and subtypes; and refine our understanding of relapsed disease. In addition, we use expression signatures to classify tumors for TP53 and NF1 pathway inactivation. We anticipate that these data will serve as a resource for pediatric oncology drug development and will guide rational clinical trial design for children with cancer