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Christopher Schofield

Researcher at Ninewells Hospital

Publications -  12
Citations -  1083

Christopher Schofield is an academic researcher from Ninewells Hospital. The author has contributed to research in topics: Diabetes mellitus & Type 2 diabetes. The author has an hindex of 8, co-authored 12 publications receiving 1012 citations. Previous affiliations of Christopher Schofield include University of Dundee & Texas Biomedical Research Institute.

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Journal ArticleDOI

Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes.

Kaixin Zhou, +76 more
- 01 Feb 2011 - 
TL;DR: It is concluded that ATM, a gene known to be involved in DNA repair and cell cycle control, plays a role in the effect of metformin upstream of AMP-activated protein kinase, and variation in this gene alters glycemic response to meetformin.

Common variants near ATM are associated with glycemic response to metformin in type 2 diabetes

Kaixin Zhou, +76 more
TL;DR: A genome-wide association study for glycemic response to metformin in 1,024 Scottish individuals with type 2 diabetes with replication in two cohorts including 1,783 Scottish individuals and 1,113 individuals from the UK Prospective Diabetes Study.
Journal ArticleDOI

Mortality and hospitalization in patients after amputation: A comparison between patients with and without diabetes

TL;DR: After LEA, patients with diabetes have an increased risk of death compared with nondiabetic patients, and efforts should be made to minimize these risks with aggressive treatment of cardiovascular risk factors and management of cardiac failure.
Journal ArticleDOI

Decreasing amputation rates in patients with diabetes-a population-based study.

TL;DR: To assess the changing rate of amputation in patients with diabetes over a 7‐year period, a large number of patients diagnosed with diabetes have had at least one amputation.
Journal ArticleDOI

Disordered insulin secretion in the development of insulin resistance and Type 2 diabetes.

TL;DR: In this paper, the potential initiating defects in Type 2 diabetes, normal pulsatile insulin secretion and the effects that disordered secretion may have on both β-cell function and hepatic insulin sensitivity are discussed.