The RNA helicase p68 (DDX5) as a selective modulator of p53-dependent cell cycle arrest and apoptosis

p68 (DDX5) is a prototypic member of the DEAD box family of RNA helicases that can unwind RNA in a context-selective and ATP-dependent manner. p68 is a multi-functional protein known to be involved in several cellular processes requiring manipulation of RNA structures, including transcription and processing of pre-mRNA, rRNA, and miRNA.

Drug safety and improving primary care prescribing safety

Prescription drugs are high-benefit but also high-risk for patients. However, the harms of treatment are often poorly quantified by the randomised controlled trials that define benefit and these trials often exclude the majority of real-world patients with target conditions because of higher risk of harm. This creates the need for observational research to quantify the risks of drugs in real-world populations (pharmaco-epidemiology). Even for drugs where the risks are well-known, we have shown that high-risk prescribing is common.

Clinical gait analysis of patients with cerebral palsy using musculoskeletal computer modelling techniques

Patients with cerebral palsy (CP) usually have muscle weakness resulting in poor muscle control, which makes walking difficult. Given that any clinical intervention aims to improve muscle control, it is crucial to monitor the changes in the muscles during gait. To date however, there has been no means with which to measure muscle characteristics (e.g. muscle force and work) directly and effectively, especially during walking, due to both technological and ethical reasons.

Analysis of the molecular basis of individuality in RTK pathway expression in human ovarian tumours – identification of patient selection biomarkers for personalised cancer medicine

Growth factors (e.g. EGF, FGF, PDGF, VEGF) and associated receptor tyrosine kinases (RTKs) regulate key signal transduction pathways which are frequently dysregulated in cancer. RTK pathways are common targets in chemotherapy drug development, but optimal patient selection and drug efficacy is often limited by lack of target specificity.

An investigation into cognitive dysfunction in honeybees and bumblebees as models for human neurodegenerative disease

The incidence of neurodegenerative disease is expected to become a major social and economical burden on society as the world’s population ages. There are no animal models that permit an investigation into both higher cognitive function and social interaction. One recently identified model is the use of bee colonies that exist as large (60,000 for honeybees) social communities where decisions are made democratically and bees communicate constantly.

Novel leptin based therapies to treat neurodegenerative disease.

Alzheimer’s disease (AD) is a progressive brain disorder resulting in profound cognitive and memory impairments. Clinical studies indicate that diet and lifestyle are key risk factors for developing neurodegenerative disorders like AD. Metabolic imbalance is also implicated in AD. Recent studies have linked the metabolic hormone, leptin to an increased incidence of AD. Consequently, leptin dysfunction may be a key factor in AD pathogenesis. Thus leptin-based therapies may prove beneficial in treating AD.

The regulation of oncogenic signalling through the Ras/MAP kinase pathway by dual-specificity protein phosphatases

Signalling through the classical Ras/ERK MAP kinase pathway is implicated in the genesis and progression of human tumours carrying activating mutations is upstream pathway effectors such as receptor tyrosine kinases and the Ras family of cellular proto-oncogenes.

Spatial feedback controls during mitosis

Background: Two principle surveillance mechanisms have evolved to guard against errors during chromosome segregation. The mitotic checkpoint delays mitosis until each and every sister chromatid has achieved stable attachment to spindle microtubules (via a protein complex known as the kinetochore), and the microtubule error-correction pathway guides this attachment process by ensuring it remains free of errors. In spite of these safeguards, the majority of tumours still manage to continually missegregate their genome.


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