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1. A multitiered analysis platform for genome sequencing: Design and initial findings of the Australian Genomics Cardiovascular Disorders Flagship

2. Effects of hospital facilities on patient outcomes after cancer surgery: an international, prospective, observational study

3. Quantitative 3D analysis and visualization of cardiac fibrosis by microcomputed tomography

4. An image analysis protocol using CellProfiler for automated quantification of post-ischemic cardiac parameters

5. VPOT: A Customizable Variant Prioritization Ordering Tool for Annotated Variants

6. NKX2-5 mutations causative for congenital heart disease retain functionality and are directed to hundreds of targets

7. Effects of hospital facilities on patient outcomes after cancer surgery

8. New cases that expand the genotypic and phenotypic spectrum of Congenital NAD Deficiency Disorder

9. Functional genomics and gene-environment interaction highlight the complexity of congenital heart disease caused by Notch pathway variants

10. VPOT: A Customizable Variant Prioritization Ordering Tool for Annotated Variants

11. Identification of clinically actionable variants from genome sequencing of families with congenital heart disease

12. Global variation in postoperative mortality and complications after cancer surgery: a multicentre, prospective cohort study in 82 countries

13. Heterozygous loss of WBP11 function causes multiple congenital defects in humans and mice

14. Functional characterization of a novel PBX1 de novo missense variant identified in a patient with syndromic congenital heart disease

15. The promises and challenges of exome sequencing in familial, non-syndromic congenital heart disease

16. Bi-allelic Mutations in NADSYN1 Cause Multiple Organ Defects and Expand the Genotypic Spectrum of Congenital NAD Deficiency Disorders

17. KIAA1217: A novel candidate gene associated with isolated and syndromic vertebral malformations

18. Gene-environment interaction impacts on heart development and embryo survival

19. Identification of clinically actionable variants from genome sequencing of families with congenital heart disease

20. A screening approach to identify clinically actionable variants causing congenital heart disease in exome data

21. Gene–environment interaction demonstrates the vulnerability of the embryonic heart

22. Loss of Cited2 causes congenital heart disease by perturbing left–right patterning of the body axis

23. A cell autonomous role for the Notch ligand Delta‐like 3 in αβ T‐cell development

24. Notch inhibition by the ligand Delta-Like 3 defines the mechanism of abnormal vertebral segmentation in spondylocostal dysostosis

25. Gestational stress induces the unfolded protein response resulting in heart defects

26. Disruption of the somitic molecular clock causes abnormal vertebral segmentation

27. NKX2-5 mutations causative for congenital heart disease retain functionality and are directed to hundreds of targets

28. Author response: NKX2-5 mutations causative for congenital heart disease retain functionality and are directed to hundreds of targets

29. Mutation of the LUNATIC FRINGE Gene in Humans Causes Spondylocostal Dysostosis with a Severe Vertebral Phenotype

30. The Mouse Homeobox Gene,Gbx2:Genomic Organization and Expression in Pluripotent Cellsin Vitroandin Vivo

31. Cited2 is required in trophoblasts for correct placental capillary patterning

32. Differential, dominant activation and inhibition of Notch signalling and APP cleavage by truncations of PSEN1 in human disease

33. A mechanism for gene-environment interaction in the etiology of congenital scoliosis

34. Cooperation between somatic Ikaros and Notch1 mutations at the inception of T-ALL

35. Role of Delta-like-3 in mammalian somitogenesis and vertebral column formation

36. Role of Delta-Like-3 in Mammalian Somitogenesis and Vertebral Column Formation

37. High levels of Notch signaling down-regulate Numb and Numblike

38. Recording Notch signaling in real time

39. Notch signaling in development and disease

40. Functional Notch signaling is required for BMP4-induced inhibition of myogenic differentiation

41. CRTR-1, a developmentally regulated transcriptional repressor related to the CP2 family of transcription factors

42. Formation of a primitive ectoderm like cell population, EPL cells, from ES cells in response to biologically derived factors

44. Notch1 endocytosis is induced by ligand and is required for signal transduction

46. A CADASIL-mutated Notch 3 receptor exhibits impaired intracellular trafficking and maturation but normal ligand-induced signaling

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