About: Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i

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About: Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i Goto Sponge NotDistinct Permalink

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description	article (en) հոդված (hy) wetenschappelijk artikel (nl) наукова стаття, опублікована у вересні 2006 (uk) im September 2006 veröffentlichter wissenschaftlicher Artikel (de)
publication date	wds:Q57920434-F8E6A75B-F182-4C84-8F2F-DD0A48DB09FF
publication date	2006-09-19 00:00:00Z (xsd:dateTime)
exact match	wds:Q57920434-931F9C7F-0351-457E-B5CB-6E4275A32ABC
exact match	https://scigraph.springernature.com/pub.10.1007/s00125-006-0407-0
cites work	wds:Q57920434-08BB9555-7295-48EE-B0AE-B17C8C9978B8 wds:Q57920434-166023B8-73C8-48A7-9D9B-C800E24C7DF8 wds:Q57920434-2709C209-5592-47A3-A563-90A85E9B1CC7 wds:Q57920434-353F5BD7-8CCF-4884-AE51-146AEFA1AF50 wds:Q57920434-358A23BB-45A9-436B-8233-E8EBC0A2CE79 wds:Q57920434-5385BD17-5EF2-47AB-97C0-C93E46E4DD44 wds:Q57920434-5E6E4B7D-4850-451C-A12B-2785984E5654 wds:Q57920434-5F190CBE-D7DC-4F39-BB82-0452E6D21363 wds:Q57920434-6D0AADD2-B27E-4E42-966A-8D4483432348 wds:Q57920434-8EC26DEB-6D1F-40A7-9238-B014D1774AD5 wds:Q57920434-A2B8936E-B82E-495C-9198-411A4204D165 wds:Q57920434-A4925726-C2DC-40CC-9652-79D7A9B2E74C wds:Q57920434-A4999B09-6EA8-490F-A6C6-68137346BBAE wds:Q57920434-AE5ED2F1-C1A5-4A69-902C-526E1B2A7395 wds:Q57920434-D1B58065-509C-4447-A2A4-79D3C99D6654 wds:Q57920434-D5658C98-B96E-46A4-AAE0-7CA0A4405F0E wds:Q57920434-D9EAAAE3-8201-481C-9965-D7E254D4C876 wds:Q57920434-E18B2153-1E8F-4B9B-A980-48D49C3B90E0 wds:Q57920434-E3757DBB-F395-4D0B-8058-26A7B8E6E408 wds:Q57920434-EA167416-72B0-4F99-8201-6F85FE66E5CD wds:Q57920434-F7B5C4B1-799A-447E-A38A-FDA91EA5A4FB wds:Q57920434-F8253ABF-4BC4-4762-BAAF-CD1D8A37A41A
cites work	Sulphonylurea action revisited: the post-cloning era. Efflux transport of tolbutamide across the blood-brain barrier. Activating mutations in Kir6.2 and neonatal diabetes: new clinical syndromes, new scientific insights, and new therapy Activating mutations in the gene encoding the ATP-sensitive potassium-channel subunit Kir6.2 and permanent neonatal diabetes Relapsing diabetes can result from moderately activating mutations in KCNJ11. Triggering and amplifying pathways of regulation of insulin secretion by glucose Permanent neonatal diabetes due to mutations in KCNJ11 encoding Kir6.2: patient characteristics and initial response to sulfonylurea therapy Molecular basis of Kir6.2 mutations associated with neonatal diabetes or neonatal diabetes plus neurological features High-dose glibenclamide can replace insulin therapy despite transitory diarrhea in early-onset diabetes caused by a novel R201L Kir6.2 mutation Glibenclamide treatment in permanent neonatal diabetes mellitus due to an activating mutation in Kir6.2. Activation of ATP-sensitive K+ channels in the ventromedial hypothalamus amplifies counterregulatory hormone responses to hypoglycemia in normal and recurrently hypoglycemic rats Hypoglycaemia and cognitive function. UKPDS 26: Sulphonylurea failure in non-insulin-dependent diabetic patients over six years. UK Prospective Diabetes Study (UKPDS) Group. Hypoglycemia in children with type 1 diabetes mellitus. Risk factors, cognitive function, and management Glucose-receptive neurones in the rat ventromedial hypothalamus express KATP channels composed of Kir6.1 and SUR1 subunits. The epidemiology of the epilepsies in children Hypothalamic ATP-sensitive K + channels play a key role in sensing hypoglycemia and triggering counterregulatory epinephrine and glucagon responses Mutations in the Kir6.2 subunit of the KATP channel and permanent neonatal diabetes: new insights and new treatment The identification of a R201H mutation in KCNJ11, which encodes Kir6.2, and successful transfer to sustained-release sulphonylurea therapy in a subject with neonatal diabetes: evidence for heterogeneity of beta cell function among carriers of the R2 Transient neonatal diabetes mellitus is associated with a recurrent (R201H) KCNJ11 (KIR6.2) mutation. Chronic exposure to tolbutamide and glibenclamide impairs insulin secretion but not transcription of K(ATP) channel components Hypoglycemia in childhood: long-term effects
author name string	wds:Q57920434-279037F2-9450-4B05-B675-FDC228F9BB3B wds:Q57920434-3EADF2F1-7B0D-4374-A965-97AAF043C3FF wds:Q57920434-5E4911B9-F5DA-44E8-8DBE-08673939C601 wds:Q57920434-7D9A6F44-8CAA-430C-93A8-36F31F0BB484 wds:Q57920434-F5393E35-0F0C-4C0E-9AB1-39ADC00E99E3
author name string	A. S. Slingerland A. T. Hattersley G. J. Bruining M. Hadders-Algra R. Nuboer
rdfs:label	Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i (en) Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i (nl)
skos:prefLabel	Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i (en) Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i (nl)
name	Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i (en) Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i (nl)
title	wds:Q57920434-2E6C45CC-59FF-4F36-8C5E-C6E625670D04
title	Improved motor development and good long-term glycaemic control with sulfonylurea treatment in a patient with the syndrome of intermediate developmental delay, early-onset generalised epilepsy and neonatal diabetes associated with the V59M mutation i (en)
page(s)	wds:Q57920434-5779004F-5302-4E55-979C-11D677507739
page(s)	2559-2563
instance of	wds:Q57920434-F844AC57-594E-4081-B70D-9507C436E52D
instance of	scholarly article
main subject	wds:Q57920434-0C213680-FDDA-40FE-8610-FB80C9C4BDFB
main subject	Patients
PubMed ID	wds:Q57920434-D45F937F-87C5-4243-8D19-0AEFC67161FF
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/17047922
PubMed ID	17047922
published in	wds:Q57920434-D5E8CD8C-88D2-47BE-9076-24614815B769
published in	Diabetologia
issue	wds:Q57920434-0F9AFF94-E9C2-4DC1-BA40-4BDD1D166578
volume	wds:Q57920434-FADC13CD-6564-4DAB-9292-79E3D0043DB0
issue	11
volume	49
DOI	wds:Q57920434-CBD80F4B-0DF5-494D-BC82-1786332F8DE1
DOI	http://dx.doi.org/10.1007/S00125-006-0407-0
DOI	10.1007/S00125-006-0407-0
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q57920434
is cites work of	Monogenic diabetes in children and young adults: Challenges for researcher, clinician and patient Systemic Administration of Glibenclamide Fails to Achieve Therapeutic Levels in the Brain and Cerebrospinal Fluid of Rodents Switching to sulphonylureas in children with iDEND syndrome caused by KCNJ11 mutations results in improved cerebellar perfusion Expression of an activating mutation in the gene encoding the KATP channel subunit Kir6.2 in mouse pancreatic beta cells recapitulates neonatal diabetes Permanent neonatal diabetes due to activating mutations in ABCC8 and KCNJ11. Glyburide ameliorates motor coordination and glucose homeostasis in a child with diabetes associated with the KCNJ11/S225T, del226-232 mutation Successful transfer to sulfonylurea therapy in an infant with developmental delay, epilepsy and neonatal diabetes (DEND) syndrome and a novel ABCC8 gene mutation Muscle dysfunction caused by a KATP channel mutation in neonatal diabetes is neuronal in origin Glibenclamide unresponsiveness in a Brazilian child with permanent neonatal diabetes mellitus and DEND syndrome due to a C166Y mutation in KCNJ11 (Kir6.2) gene

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