Results 61 to 70 of about 6,169 (207)

What neonatal complications should the pediatrician be aware of in case of maternal gestational diabetes? [PDF]

open access: yes, 2015
In the epidemiologic context of maternal obesity and type 2 diabetes (T2D), the incidence of gestational diabetes has significantly increased in the last decades.
Mitanchez, D.   +2 more
core   +1 more source

Opening closed inward rectifier potassium channel doors

open access: yesBritish Journal of Pharmacology, Volume 183, Issue 10, Page 2197-2218, May 2026.
Inwardly rectifying potassium (KIR) channels are essential regulators of membrane potential in excitable and non‐excitable tissues. Although KIR channels exhibit a biophysical preference for potassium influx due to voltage‐dependent block of outward current by polyamines and Mg2+, under physiological conditions, they predominantly mediate K+ efflux ...
Anna Stary‐Weinzinger   +3 more
wiley   +1 more source

Congenital hyperinsulinism: current status and future perspectives [PDF]

open access: yesAnnals of Pediatric Endocrinology & Metabolism, 2014
The diagnosis and treatment of congenital hyperinsulinism (CHI) have made a remarkable progress over the past 20 years and, currently, it is relatively rare to see patients who are left with severe psychomotor delay.
Tohru Yorifuji
doaj   +1 more source

Congenital hyperinsulinism caused by a de novo mutation in the ABCC8 gene: a case report [PDF]

open access: yes, 2018
K
Balogh, István   +5 more
core  

Transjugular Leadless Pacemaker Implantation in an Adolescent With Central Hypoventilation Syndrome: A Case Report

open access: yesPacing and Clinical Electrophysiology, Volume 49, Issue 5, Page 606-609, May 2026.
ABSTRACT Background Permanent pacing in pediatric patients is complicated by small body size, vascular access limitations, and the need for durable long‐term management. Leadless pacemakers offer an emerging alternative that minimizes infection and lead‐related complications, yet vascular access remains a key challenge in young patients.
Marzia Giaccardi   +4 more
wiley   +1 more source

Extreme caution on the use of sirolimus for the congenital hyperinsulinism in infancy patient

open access: yesOrphanet Journal of Rare Diseases, 2017
We have recently published on the limited effectiveness of sirolimus as a treatment option for hypoglycaemia as a consequence of hyperinsulinism. Our data oppose the view that mTOR inhibitors provide new opportunities for the treatment of patients with ...
Indraneel Banerjee   +2 more
doaj   +1 more source

Thyroxine-binding globulin: investigation of microheterogeneity [PDF]

open access: yes, 1981
Preparations of T4-binding globulin (TBG) from human serum was performed using only two affinity chromatography steps. Purity of the protein was demonstrated by a single band in overloaded disc and sodium dodecyl sulfate electrophoresis, equimolar ...
Gärtner, Roland   +4 more
core   +1 more source

A Case Series: Congenital Hyperinsulinism [PDF]

open access: yesInternational Journal of Endocrinology and Metabolism, 2016
Congenital hyperinsulinism is a rare inherited disease caused by mutations in genes responsible for β-cell's function in glucose hemostasis leading to profound and recurrent hypoglycemia. The incidence of the disease is about 1 in 50000 newborns. Mutations in at least 8 genes have been reported to cause congenital hyperinsulinism.
Alaei, Mohammad Reza   +3 more
openaire   +2 more sources

Contrasting Effects of Chronic Glucokinase Activation and Inhibition on Pancreatic Beta‐Cell Function

open access: yesThe FASEB Journal, Volume 40, Issue 7, 15 April 2026.
In the non‐diabetic beta‐cell (top left) activation of glucokinase (bottom left) leads to inhibition of mitochondrial metabolism and thereby impairs insulin secretion. The effect is similar to that of chronic hyperglycaemia as seen in the diabetic beta‐cell (top right).
Matthew Lloyd   +9 more
wiley   +1 more source

Regulation of metabolism by miR-378 [PDF]

open access: yes, 2014
The present invention provides a method of regulating fatty acid metabolism in a cell by contacting the cell with a modulator of miR-378 and/or miR-378* activity or expression.
Carrer, Michele, Olson, Eric N.
core   +1 more source

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