Hyperglycaemia-induced impairment of the autorhythmicity and gap junction activity of mouse embryonic stem cell-derived cardiomyocyte-like cells.

Diabetes mellitus with hyperglycaemia is a major risk factor for malignant cardiac dysrhythmias. However, the underlying mechanisms remain unclear, especially during the embryonic developmental phase of the heart. This study investigated the effect of hyperglycaemia on the pulsatile activity of stem cell-derived cardiomyocytes.

Organisational alteration of cardiac myofilament proteins by hyperglycaemia in mouse embryonic stem cell-derived cardiomyocytes.

The exposure of the developing foetal heart to hyperglycaemia in mothers with diabetes mellitus is a major risk factor for foetal cardiac complications that lead to heart failure. We studied the effects of hyperglycaemia on the layout of cardiac myofilament proteins in stem cell-derived cardiomyocytes and their possible underlying mechanisms. Mouse embryonic stem cells (mESCs) were differentiated into cardiac-like cells and cultured in media containing baseline- or high glucose concentrations.

Hyperglycaemia-Induced Contractile Dysfunction and Apoptosis in Cardiomyocyte-Like Pulsatile Cells Derived from Mouse Embryonic Stem Cells.

Hyperglycaemia, a key metabolic abnormality in diabetes mellitus, is implicated in pathological cardiogenesis during embryological development. However, the underlying mechanisms and potential therapeutic targets remain unknown. We, therefore, studied the effect of hyperglycaemia on mouse embryonic stem cell (mESC) cardiac differentiation.

Molecular and electrophysiological features of spinocerebellar ataxia type seven in induced pluripotent stem cells.

Spinocerebellar ataxia type 7 (SCA7) is an inherited neurodegenerative disease caused by a polyglutamine repeat expansion in the ATXN7 gene. Patients with this disease suffer from a degeneration of their cerebellar Purkinje neurons and retinal photoreceptors that result in a progressive ataxia and loss of vision. As with many neurodegenerative diseases, studies of pathogenesis have been hindered by a lack of disease-relevant models.

CYP3A5 genotypes and risk of oesophageal cancer in two South African populations.

CYP3A5 is the major cytochrome P450 enzyme in the oesophagus and metabolises many potentially carcinogenic compounds. The frequencies of CYP3A5 allelic variants, CYP3A5*2, *3, *6 and *7 which code for enzymes with severely decreased activities were compared between 241 oesophageal cancer patients and 272 controls in Black and Mixed Ancestry South Africans. A significantly higher frequency of CYP3A5*3 was observed in the controls compared to patients amongst the Mixed Ancestry group (P=0.

Genotyping of alcohol dehydrogenase type 2 and 3 using a two-buffer polyacrylamide gel electrophoresis system.

Genetic polymorphisms in the alcohol dehydrogenase genes, ADH2 and ADH3, have been shown to affect individual susceptibility to diseases such as alcoholism and oesophageal cancer. Although several PCR-based methods for genotyping these enzymes have been previously developed, the two-buffer polyacrylamide gel electrophoresis system has the ability to rapidly resolve all classes of point mutations within 2-3 hours instead of the conventional overnight separation. The success of this technique is partly attributable to a discontinuous two-phase buffer system and horizontal flatbed gel electrophoresis rather than conventional vertical gels.