Effectiveness of a digital health and financial incentive intervention to promote physical activity in patients with type 2 diabetes: study protocol for a randomised controlled trial with a nested qualitative study-ACTIVATE trial.

Background: The prevention of type 2 diabetes (T2DM) is recognised as a health care priority in the UK. In people living with T2DM, lifestyle changes (e.g.

Risk of second brain tumour after radiotherapy for pituitary adenoma or craniopharyngioma: a retrospective, multicentre, cohort study of 3679 patients with long-term imaging surveillance.

Background: Radiotherapy is a valuable treatment in the management algorithm of pituitary adenomas and craniopharyngiomas. However, the risk of second brain tumour following radiotherapy is a major concern. We assessed this risk using non-irradiated patients with the same primary pathology and imaging surveillance as controls.

Loss of ZnT8 function protects against diabetes by enhanced insulin secretion.

A rare loss-of-function allele p.Arg138* in SLC30A8 encoding the zinc transporter 8 (ZnT8), which is enriched in Western Finland, protects against type 2 diabetes (T2D). We recruited relatives of the identified carriers and showed that protection was associated with better insulin secretion due to enhanced glucose responsiveness and proinsulin conversion, particularly when compared with individuals matched for the genotype of a common T2D-risk allele in SLC30A8, p.

Insulin inhibits glucagon release by SGLT2-induced stimulation of somatostatin secretion.

Hypoglycaemia (low plasma glucose) is a serious and potentially fatal complication of insulin-treated diabetes. In healthy individuals, hypoglycaemia triggers glucagon secretion, which restores normal plasma glucose levels by stimulation of hepatic glucose production. This counterregulatory mechanism is impaired in diabetes.

Electrophysiological properties of human beta-cell lines EndoC-βH1 and -βH2 conform with human beta-cells.

Limited access to human islets has prompted the development of human beta cell models. The human beta cell lines EndoC-βH1 and EndoC-βH2 are increasingly used by the research community. However, little is known of their electrophysiological and secretory properties.

Does Islet Size Really Influence Graft Function After Clinical Islet Transplantation?

Background: It has been proposed that islet transplants comprised primarily of small rather than large islets may provide better graft function, due to their lower susceptibility to hypoxic damage. Our aim was to determine whether islet size correlated with in vivo graft function in islet transplant recipients with C peptide-negative type 1 diabetes when islets have undergone pretransplant islet culture.

Methods: Human pancreatic islets were isolated, cultured for 24 hours and infused by standardized protocols.

α-cell glucokinase suppresses glucose-regulated glucagon secretion.

Glucagon secretion by pancreatic α-cells is triggered by hypoglycemia and suppressed by high glucose levels; impaired suppression of glucagon secretion is a hallmark of both type 1 and type 2 diabetes. Here, we show that α-cell glucokinase (Gck) plays a role in the control of glucagon secretion. Using mice with α-cell-specific inactivation of Gck (αGckKO mice), we find that glucokinase is required for the glucose-dependent increase in intracellular ATP/ADP ratio and the closure of K channels in α-cells and the suppression of glucagon secretion at euglycemic and hyperglycemic levels.

δ-cells and β-cells are electrically coupled and regulate α-cell activity via somatostatin.

Key Points: We used a mouse expressing a light-sensitive ion channel in β-cells to understand how α-cell activity is regulated by β-cells. Light activation of β-cells triggered a suppression of α-cell activity via gap junction-dependent activation of δ-cells. Mathematical modelling of human islets suggests that 23% of the inhibitory effect of glucose on glucagon secretion is mediated by β-cells via gap junction-dependent activation of δ-cells/somatostatin secretion.

Reversible changes in pancreatic islet structure and function produced by elevated blood glucose.

Diabetes is characterized by hyperglycaemia due to impaired insulin secretion and aberrant glucagon secretion resulting from changes in pancreatic islet cell function and/or mass. The extent to which hyperglycaemia per se underlies these alterations remains poorly understood. Here we show that β-cell-specific expression of a human activating KATP channel mutation in adult mice leads to rapid diabetes and marked alterations in islet morphology, ultrastructure and gene expression.

Adjuvant perioperative intraperitoneal chemotherapy in locally advanced colorectal carcinoma: preliminary results.

Background and Aims. Intraperitoneal chemotherapy is a basic tool in the treatment of peritoneal malignancy. The purpose of the study is to investigate the effect of adjuvant perioperative intraperitoneal chemotherapy in the treatment of locally advanced colorectal cancer.

Real-time computation of two-dimensional moments on binary images using image block representation.

This work presents a new approach and an algorithm for binary image representation, which is applied for the fast and efficient computation of moments on binary images. This binary image representation scheme is called image block representation, since it represents the image as a set of nonoverlapping rectangular areas. The main purpose of the image block representation process is to provide an efficient binary image representation rather than the compression of the image.

The Emery-Dreifuss muscular dystrophy associated-protein emerin is phosphorylated on serine 49 by protein kinase A.

Emerin is a ubiquitously expressed inner nuclear membrane protein of unknown function. Mutations in its gene give rise to X-linked Emery-Dreifuss muscular dystrophy (X-EDMD), a neuromuscular condition with an associated life-threatening cardiomyopathy. We have previously reported that emerin is phosphorylated in a cell cycle-dependent manner in human lymphoblastoid cell lines [Ellis et al.