Social Media and Website Use: The Experiences of Parents and Carers Accessing Care at the Oxford Craniofacial Unit.

Introduction: Historically, medical professionals have been the providers of specialist information about rare medical conditions. Now, increasingly, patients and the public are using the internet to access and generate information about medical diagnoses. The global nature of the internet allows patients to connect across geographical borders, and to obtain and share information that would have been previously inaccessible to them.

The role of the clinical psychologist within a cleft service.

Clinical psychologists are core members of UK cleft services. This paper outlines the variety of ways in which clinical psychologists work across the lifespan to promote the psychological wellbeing of those born with a cleft and their families. In the context of dental or orthodontic treatment, this involves a combination of early intervention and advice, psychological assessment or specialist psychological therapy for individuals experiencing dental anxiety or anxiety regarding the appearance of their teeth.

PARP1-MGMT complex underpins pathway crosstalk in O-methylguanine repair.

DNA lesions induced by alkylating agents are repaired by two canonical mechanisms, base excision repair dependent on poly(ADP) ribose polymerase 1 (PARP1) and the other mediated by O-methylguanine (OmeG)-DNA methyltransferase (MGMT) in a single-step catalysis of alkyl-group removal. OmeG is the most cytotoxic and mutagenic lesion among the methyl adducts induced by alkylating agents. Although it can accomplish the dealkylation reaction all by itself as a single protein without associating with other repair proteins, evidence is accumulating that MGMT can form complexes with repair proteins and is highly regulated by a variety of post-translational modifications, such as phosphorylation, ubiquitination, and others.

Mitochondrial TrxR2 regulates metabolism and protects from metabolic disease through enhanced TCA and ETC function.

Mitochondrial dysfunction is a key driver of diabetes and other metabolic diseases. Mitochondrial redox state is highly impactful to metabolic function but the mechanism driving this is unclear. We generated a transgenic mouse which overexpressed the redox enzyme Thioredoxin Reductase 2 (TrxR2), the rate limiting enzyme in the mitochondrial thioredoxin system.