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Helge Ræder's picture

Helge Ræder

Professor, Vice Dean for Innovartion at Faculty of Medicine, Consultant Pediatrician
  • E-mailHelge.Rader@uib.no
  • Phone+47 478 92 554
  • Visitor Address
    Dept of Pediatrics, Haukeland University Hospital
    5020 Bergen
    Room 
    3010 TEL 55975263
  • Postal Address
    Postboks 7804
    5020 Bergen

My research aim is to characterize and better understand the major signaling pathways involved in endocrine disease, specifically diabetes development and adreno-gonadal development, by studying developing cells differentiated from induced pluripotent stem cells (iPSCs) generated from families with monogenic disease.

https://raederlab.wordpress.com/

http://www.uib.no/diabetes/80059/node-6-stamcelleforskning

I teach pediatric topics to medical students, including lectures and bedside teaching. My lectures include Growth and Puberty Disorders (MED12) and Intoxication and Fluid Therapy (MED9) (Department of Clinical Science). 

I also teach metabolic diseases for Nutrition students (NUC352, Department of Clinical Medicine).

I also contribute to teaching in Master Courses (BMED330; Department of Biomedicine).

I also lead two Elective Courses at the Medical Faculty (Department of Clinical Science):

ELMED303 (Future Medicine)

ELMED223 (Innovation and Entrepeneurship)

I also organize and teach pediatric residents at the Course in Pediatric Endocrinology with topics including Calcium metabolism and case demonstrations.

https://scholar.google.com/citations?user=ecPm_OoAAAAJ&hl=en

  • 2020. Encapsulation boosts islet-cell signature in differentiating human induced pluripotent stem cells via integrin signalling . Scientific Reports.
  • 2020. Bioinformatic analyses of miRNA-mRNA signature during hiPSC differentiation towards insulin-producing cells upon HNF4α mutation. Biomedicines. 1-20.
  • 2019. The effect of WnT pathway modulators on human iPSC-derived pancreatic beta cell maturation. Frontiers in Endocrinology. 1-13.
  • 2019. Reprogrammed cells display distinct proteomic signaturesAssociated with colony morphology variability. Stem Cells International. 1-16.
  • 2019. In vivo hyperglycemia exposure elicits distinct period-dependent effects on human pancreatic progenitor differentiation, conveyed by oxidative stress. Acta Physiologica. 1-16.
  • 2019. HNF4A haploinsufficiency in MODY1 abrogates liver and pancreas differentiation from patient-derived induced pluripotent stem cells. iScience. 192-205.
  • 2019. Encapsulation boosts islet-cell signature in differentiating human induced pluripotent stem cells via integrin signalling. bioRxiv - the preprint server for biology.
  • 2019. Dynamic proteome profiling of human pluripotent stem cell-derived pancreatic progenitors. Stem Cells.
  • 2019. Diabetes relief in mice by glucose-sensing insulin-secreting human α-cells. Nature. 43-48.
  • 2018. The role of the carboxyl ester lipase (CEL) gene in pancreatic disease. 12-19.
  • 2018. Springboard to an academic career - A national medical student research program. PLOS ONE. 1-8.
  • 2017. Probing the missing mature β-cell proteomic landscape in differentiating patient iPSC-derived cells. Scientific Reports. 1-14.
  • 2017. Anatomy and evolution of database search engines—a central component of mass spectrometry based proteomic workflows. 292-306.
  • 2016. Using Proteomics Bioinformatics Tools and Resources in Proteogenomic Studies. Advances in Experimental Medicine and Biology. 65-75.
  • 2016. Systemic Analysis of Regulated Functional Networks. Methods in molecular biology. 287-310.
  • 2016. Hereditary hypophosphatemia in Norway: A retrospective population-based study of genotypes, phenotypes, and treatment complications. European Journal of Endocrinology. 125-136.
  • 2016. Exploring the potential of public proteomics data. 214-225.
  • 2016. Early Developmental Perturbations in a Human Stem Cell Model of MODY5/HNF1B Pancreatic Hypoplasia. Stem Cell Reports. 357-367.
  • 2015. The chromosome 9p21 CVD- and T2D-associated regions in a Norwegian population (the HUNT2 survey). 9 pages.
  • 2014. Long-term clinical outcome and phenotypic variability in hyperphosphatemic familial tumoral calcinosis and hyperphosphatemic hyperostosis syndrome caused by a novel GALNT3 mutation; case report and review of the literature. BMC Genetics.
  • 2014. Carboxyl-ester lipase maturity-onset diabetes of the young is associated with development of pancreatic cysts and upregulated MAPK signaling in secretin-stimulated duodenal fluid. Diabetes. 259-269.
  • 2014. Carboxyl-ester lipase maturity-onset diabetes of the young disease protein biomarkers in secretin-stimulated duodenal juice. Journal of Proteome Research. 521-530.
  • 2013. Severe pancreatic dysfunction but compensated nutritional status in monogenic pancreatic disease caused by carboxyl-ester lipase mutations. Pancreas. 1078-1084.
  • 2013. Monogenetic diabetes mellitus in Norway :. Norsk Epidemiologi. 55-60.
  • 2013. Exome sequencing reveals FAM20c mutations associated with fibroblast growth factor 23-related hypophosphatemia, dental anomalies, and ectopic calcification. Journal of Bone and Mineral Research. 1378-1385.
  • 2013. Exocrine pancreatic function in hepatocyte nuclear factor 1 beta-maturity-onset diabetes of the young (HNF1B-MODY) is only moderately reduced: compensatory hypersecretion from a hypoplastic pancreas. Diabetic Medicine. 946-955.
  • 2013. Derivation of Human Induced Pluripotent Stem Cells from Patients with Maturity Onset Diabetes of the Young. Journal of Biological Chemistry. 5353-5356.
  • 2013. Absence of diabetes and pancreatic exocrine dysfunction in a transgenic model of carboxyl-ester lipase-MODY (Maturity-Onset Diabetes of the young). PLOS ONE. 11 pages.
  • 2012. The role of pancreatic imaging in monogenic diabetes mellitus. 148-159.
  • 2012. Skreddersydd medisin eller narsissomikk? Tidsskrift for Den norske legeforening. 1844-1845.
  • 2012. HNF1B mutation in a Turkish child with renal and exocrine pancreas insufficiency, diabetes and liver disease. Pediatric Diabetes. e1-e5.
  • 2011. The role of pancreatic imaging in monogenic diabetes. Nature Reviews Endocrinology.
  • 2011. Evaluation of four novel genetic variants affecting hemoglobin A1c levels in a population-based type 2 diabetes cohort (the HUNT2 study). BMC Medical Genetics. 6 pages.
  • 2011. Diabetes and pancreatic exocrine dysfunction due to mutations in the carboxyl ester lipase gene-maturity onset diabetes of the young (CEL-MODY) A PROTEIN MISFOLDING DISEASE. Journal of Biological Chemistry. 34593-34605.
  • 2011. A large multi-centre European study validates high-sensitivity C-reactive protein (hsCRP) as a clinical biomarker for the diagnosis of diabetes subtypes. Diabetologia. 2801-2810.
  • 2010. Polygenic risk variants for Type 2 Diabetes susceptibility modify age at diagnosis in Monogenic HNF1A Diabetes. Diabetes. 266-271.
  • 2010. Pancreatic Function in Carboxyl-Ester Lipase Knockout Mice. Pancreatology (Print). 467-476.
  • 2010. Mutations in the VNTR of the carboxyl-ester lipase gene (CEL) are a rare cause of monogenic diabetes. Human Genetics. 55-64.
  • 2010. Fremskritt innen diabetesgenetikk. 1145-1149.
  • 2008. X-bundet hypofosfatemisk rakitt: Ny kunnskap om patofysiologi, behandling og oppfølging. Pediatrisk Endokrinologi. 70-78.
  • 2008. Structural changes in the repeated region of the carboxyl-ester lipase (CEL) gene and the development of diabetes. Diabetologia. S123-S123.
  • 2008. Reduced pancreatic volume in hepatocyte nuclear factor 1A-maturity-onset diabetes of the young. Journal of Clinical Endocrinology and Metabolism. 3505-3509.
  • 2008. Prevalence of HNF1A (MODY3) mutations in a Norwegian population (the HUNT2 Study). Diabetic Medicine. 775-781.
  • 2008. Pancreatic Exocrine Dysfunction in Maturity-Onset Diabetes of the Young Type 3. Diabetes Care. 306-310.
  • 2008. Neurological features and enzyme therapy in patients with endocrine and exocrine pancreas dysfunction due to CEL mutations. Diabetes Care. 1738-1740.
  • 2008. Mutations in the insulin gene can cause MODY and autoantibody-negative type 1 diabetes. Diabetes. 1131-1135.
  • 2008. Lack of pancreatic body and tail in HNF1B mutation carriers. Diabetic Medicine. 782-787.
  • 2008. Genetic analysis of recently identified type 2 diabetes loci in 1,638 unselected patients with type 2 diabetes and 1,858 control participants from a Norwegian population-based cohort (the HUNT study). Diabetologia. 971-977.
  • 2008. Diagnostic screening of MODY2/GCK mutations in the Norwegian MODY Registry. Pediatric Diabetes. 442-449.
  • 2008. A case of X-linked hypophosphatemic rickets: complications and the therapeutic use of cinacalcet. European Journal of Endocrinology. 101-105.
  • 2007. Studies in 3,523 Norwegians and meta-analysis in 11,571 subjects indicate that variants in the hepatocyte nuclear factor 4 alpha (HNF4A) P2 region are associated with type 2 diabetes in Scandinavians. Diabetes. 3112-3117.
  • 2007. Pancreatic lipomatosis is a structural marker in nondiabetic children with mutations in carboxyl-Ester lipase. Diabetes. 444-449.
  • 2007. Pancreatic exocrine deficiency is common in MODY 3. Diabetologia. S123-S123.
  • 2006. Ny type diabetes. Diabetesforum. 20-21.
  • 2006. Novel monogenic causes of diabetes and pancreatic exocrine dysfunction.
  • 2006. Mutations in the CEL VNTR cause a syndrome of diabetes and pancreatic exocrine dysfunction. Nature Genetics. 54-62.
  • 2006. A hepatocyte nuclear factor-4 alpha gene (HNF4A) P2 promoter haplotype linked with late-onset diabetes - Studies of HNF4A variants in the Norwegian MODY registry. Diabetes. 1899-1903.
  • 2005. Molekylærgenetisk diagnostikk ved diabetes mellitus. Tidsskrift for Den norske legeforening. 2968-2972.
  • 2004. Permanent neonatal diabetes due to mutations in KCNJ11 encoding Kir6.2 - Patient characteristics and initial response to sulfonylurea therapy. Diabetes. 2713-2718.
  • 2002. Klinisk molekylærmedisin:DNA-sekvensering. Pediatrisk Endokrinologi. 51-56.
  • 1996. Unchanged 24-hour ambulatory blood pressure during short-term salt restriction and salt repletion in normotensive subjects. Blood Pressure Monitoring. 39-44.

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