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Current Filters

Funders:
The Wellcome Trust
Recipients:
University College London
Amounts:
£500 - £1,000

Results

Cartoonist-in-Residence, UCL and UCLH 13 Apr 2016

A portrayal of the experiences of UCL/H staff and their patients, as revealing and humorous stories told in the snapshot form of the cartoon. Ros Asquith will spend one day a week for a minimum of one year at UCL/H - observing meetings, presentations, the Grand Round and the wards, listening to doctors, nurses, research scientists, students, managers and administrative staff. She will then aim to capture each visit’s key experiences as cartoons. Two days already spent exploring this process produced about 30 ideas. I appreciate that the spare time of health professionals is short - fortunately, cartoons can be understood, liked, disliked or improved very quickly. Each week I would circulate by email rough sketches of ideas drawn from that week’s visit, to a representative group nominated by UCL/H. From their recommendations and thoughts, I would then develop the most successful ideas as finished artwork. I intend to run workshops, and discussions and encourage staff and patients to draw, based on my wide experience of drawing workshops with all ages. At the end of the year, the work would be exhibited, printed as postcards, leaflets, and a book. I would host a series of workshops, discussions.

Amount: £15,900
Funder: The Wellcome Trust
Recipient: University College London
Amount: £14,500
Funder: The Wellcome Trust
Recipient: University College London
Amount: £12,000
Funder: The Wellcome Trust
Recipient: University College London

UCL - Neuroscience 30 Sep 2016

Not available

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology 30 Sep 2016

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology 30 Sep 2016

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

UCL - Neuroscience 30 Sep 2016

Not available

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology 30 Sep 2016

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology 30 Sep 2016

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology 30 Sep 2016

University College London/Birkbeck Interdisciplinary Programme in Structural, Computational and Chemical Biology

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

Neuroscience 30 Sep 2016

Not available

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

UCL - Neuroscience 30 Sep 2016

Not available

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

UCL - Neuroscience 30 Sep 2016

Not available

Amount: £133,252
Funder: The Wellcome Trust
Recipient: University College London

Life history of an organizer: what determins transient orgnaizer function in Hensen's node? 30 Sep 2016

The "primary organizer" of the vertebrate embryo is a group of cells at the gastrula stage which is able to induce a complete patterned nervous system when transplanted to another site. However, the position in the embryo where the organizer is located only has these properties for a short time. This time corresponds to when two particular populations of cells ("central epiblast" and "posterior deep") come together. After this, as cells leave to form the prechordal mesendoderm, organizer ability is lost again. The aim of this project is to find out whether the organizer function of Hensen's node is the sum of properties that exist in separate cell populations or whether new properties are generated by interactions between them, and thus determine how dynamics of these cells contribute to the transient nature of organizer function. Cell dynamics will be studied using carbocyanine dye (Dil and DiO) labelling of the 'central' and 'posterior' populations to identify their contributions and roles in the organizer. These populations, individually and combined, will be assessed by studying their transcriptomes by RNA sequencing. Their organizer function will then be assessed, in time-course, by the gene expression profiles in cells receiving signals from these populations

Amount: £28,350
Funder: The Wellcome Trust
Recipient: University College London

Coordinated neural tube closure: The role of biomechanical properties in directing neuropore 30 Sep 2016

Neural tube (NT) closure is a morphogenetic event of vertebrate development that results in severe birth defects (e.g. spina bifida) when disturbed. The key genes/pathways of neurulation have been studied extensively, but many aspects of the developmental mechanisms remain unclear. This project addresses two questions: (i) how is neurulation linked mechanistically with the process of axial elongation, which accompanies spinal closure in higher vertebrates, and (ii) how/where do tissue-level biomechanical forces arise that drive NT morphogenesis? Neuro-mesodermal progenitors (NMPs) generate both neuroepithelium and mesoderm during axial elongation, and will be fate-mapped in the NT of cultured mouse embryos. Single-cell labelling by photo-conversion of cells expressing the Dendra2 construct will reveal the timing of neural commitment in NMPs. Requirement for NMPs in NT closure will be assessed in embryos mutant for Grhl3, a gene expressed in NMPs and where loss- or gain-of-function causes spina bifida. Biomechanical forces in the closing NT will be detected by electroporating a FRET-based mechanosensor that reports stress in cytoskeleton-linked proteins (e.g. alpha-actinin). Embryo manipulations (e.g. closed NT incision) will be tested for effects on FRET-reporter activity to identify the origin of closure forces, while mutant embryos developing spina bifida will be assessed for altered force distribution.

Amount: £55,346
Funder: The Wellcome Trust
Recipient: University College London

Allosteric modulators of nicotine acetylcholine receptors 30 Sep 2016

Nicotinic acetylcholine receptors (nAChRs) are major excitatory neurotransmitters and have been implicated in a number of neurological and psychiatric disorders. The primary aim of the project will be to combine synthetic organic chemistry and pharmacological techniques to examine allosteric modulation of nAChRs. This will build upon recent work in the Sheppard and Millar labs at UCL and will also exploit a refined homology model of the a7 nAChR that was generated as part of a rotation project during the first year of this PhD studentship. It is anticipated that the generation of novel compounds, combined with computer docking studies and molecular pharmacological techniques, will enable a greater insight to be gained into the mechanism of action of nAChR allosteric modulators.

Amount: £2,529
Funder: The Wellcome Trust
Recipient: University College London

Physiological roles of endogenous neurosteroids at extrasynaptic GABAARs 30 Sep 2016

The role of GABA and GABAA receptors in providing synaptic and tonic inhibition of neurons is an important aspect of normal brain function. This is evident when inhibition becomes dysfunctional, resulting in neurological and psychiatric diseases. GABA receptors are also subject to modulation by endogenous compounds. Paramount amongst these are the neurosteroids that regulate inhibition, but their physiological role and how they are involved in brain diseases is largely unexplored. Having discovered the binding site for neurosteroids on GABAA receptors, revealing a highly conserved site on receptor alpha subunits, we can now dissect both their physiological and pathophysiological roles by adopting a genetic-based approach. The main aim of this proposal is to characterise the GABA receptor alpha4 subunit in a mouse knock-in line that has been rendered insensitive to neurosteroids by mutation of its binding site. This subunit is involved in the assembly of extrasynaptic GABAA receptors. By investigating inhibitory transmission, using brain slice preparations and dissociated neuronal cell cultures, in conjunction with biochemical, chemical, electrophysiological, imaging (single particle tracking), pharmacological and molecular approaches, we will uncover the role(s) of neurosteroids at this highly sensitive extrasynaptic GABAA receptor that underpins tonic inhibition in the brain.

Amount: £30,917
Funder: The Wellcome Trust
Recipient: University College London

The role of the blood nerve barrier in peripheral neuropathies. 30 Sep 2016

The nervous system in maintained in a protective environment by a specialised vasculature. In contrast to the Blood Brain Barrier (BBB), the Blood Nerve Barrier (BNB) is poorly characterised despite having an important role in protecting peripheral nerves and its disruption being associated with neuropathies associated with pathologies such as diabetes and cancer. We have initiated a characterisation of the BNB in the sciatic nerve and have found that it is distinct from the BBB both in its permeability and cellular make-up. Moreover, we have developed a unique transgenic mouse in which ERK signalling in Schwann cells (SCs) in the nerve can reversibly open the barrier, which mimics the normal injury response. This provides a powerful model system for studying in a temporal manner how the BNB can be broken down and reformed. The aims of this proposal are threefold. 1. To characterise the nature of the BNB throughout the PNS and correlate differences with structural changes 2. To determine the role of SC-secreted Semaphorin 3A in the regulation of the BNB. 3. To analyse the expression and role of BBB transporters in the BNB.

Amount: £34,680
Funder: The Wellcome Trust
Recipient: University College London

Probing the synaptic mechanisms of human genetic neurological disorders 30 Sep 2016

We are interested in how mutations that lead to human neurological disorders (particularly epilepsy) impact neuronal function. Much of our previous work has focused on how mutations change intrinsic neuronal excitability, but epilepsy is increasingly being associated with genes which are also predicted to perturb synaptic activity, and the aim of this project is to probe whether a subset of mutations linked to similar genetic epilepsy disorders have similar consequences for pre-synaptic properties. We will develop a lentiviral tool that will express a fluorescent protein (e.g. RFP) and a cDNA or shRNA to mimic a genetic disorder in a subset of cultured neurons. Recordings will be from untransduced post-synaptic cells, limiting the possibility of post-synaptic genetic effects contaminating readouts of the impact of mutations on synaptic release. We will also investigate whether incorporation of an activating opsin is sufficient for light based stimulation of the pre-synaptic neurons only. By incorporating cellspecific promoters, this project will also allow us to test the hypothesis that mutations that cause seizures have distinct effects in interneurons and excitatory neurons, including how they couple excitation to transmitter release. This project will dissect the synaptic mechanisms of disease, and correlate them with subsets of neurons.

Amount: £5,805
Funder: The Wellcome Trust
Recipient: University College London