Christine Ferrara

ORCID: 0000-0003-0008-7751
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About
Contact & Profiles
Research Areas
  • Hyperglycemia and glycemic control in critically ill and hospitalized patients
  • Diabetes Management and Research
  • Diabetes and associated disorders
  • Circadian rhythm and melatonin
  • Adipose Tissue and Metabolism
  • Blood disorders and treatments
  • Diet, Metabolism, and Disease
  • Metabolism, Diabetes, and Cancer
  • Chronic Lymphocytic Leukemia Research
  • Body Composition Measurement Techniques
  • Chronic Myeloid Leukemia Treatments
  • Neuroblastoma Research and Treatments
  • Pancreatic function and diabetes
  • Neurobiology and Insect Physiology Research

UCSF Benioff Children's Hospital
2020

Children's Hospital of Philadelphia
2013-2016

BackgroundType 1 diabetes results from autoimmune-mediated destruction of β cells. The tyrosine kinase inhibitor imatinib might affect relevant immunological and metabolic pathways, preclinical studies show that it reverses prevents diabetes. Our aim was to evaluate the safety efficacy in preserving β-cell function patients with recent-onset type diabetes.MethodsWe did a multicentre, randomised, double-blind, placebo-controlled, phase 2 trial. Patients (<100 days diagnosis), aged 18–45...

10.1016/s2213-8587(21)00139-x article EN cc-by The Lancet Diabetes & Endocrinology 2021-06-29

Background Diabetes ketoacidosis (DKA) is a common presentation and complication of type 1 diabetes (T1D). While intravenous insulin typically used to treat acute metabolic abnormalities, the transition from subcutaneous treatment can present challenge. We hypothesize that co-administration glargine, long-acting analog, during infusion may facilitate flexible safe therapy. Objective To determine if practice administering glargine associated with an increased risk hypoglycemia, hypokalemia,...

10.1111/pedi.12462 article EN Pediatric Diabetes 2016-11-03

Abstract Background: Congenital hyperinsulinism (HI) is the leading cause of severe, persistent hypoglycemia in infants. Transient HI seen at risk neonates due to prenatal stress and some congenital cases mutations K-ATPase channel are responsive diazoxide. It not a common practice obtain genetic evaluation for diazoxide HI. However, children with dominant inactivating variants HNF4A gene may present diazoxide-responsive mimic transient infancy. Objective: To describe two siblings mutation...

10.1210/jendso/bvaa046.1205 article EN cc-by-nc-nd Journal of the Endocrine Society 2020-04-01
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