Cardiff, United Kingdom
Cardiff, United Kingdom

Cardiff University is a research university located in the Cathays Park area of Cardiff, Wales, United Kingdom. It received its Royal charter in 1883 and is a member of the Russell Group of Universities. The university is consistently recognised as providing high quality research-based university education in Wales. Wikipedia.


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Patent
University of Cardiff | Date: 2014-07-03

The present application relates to therapeutics and pharmaceutical compositions, their use and also methods for preventing post-traumatic osteoarthritis, early or late stage, using compounds which inhibit either, or both, AMPA and KA glutamate receptors (Glu Rs).


Patent
University of Cardiff | Date: 2017-04-05

A process for preparing phosphoramidates of nucleosides where a desired enantiomer, having regard to the asymmetric chiral centre of the phosphorus atom P, is provided in an enriched amount. The process comprises admixing a nucleoside with a phosphorochloridate in the presence of a catalyst comprising a metal salt selected from the group consisting of salts of Ciu Fe, La and Yb.


Patent
University of Cardiff | Date: 2017-01-11

The invention relates to a device for use in skin improvement or repair, including promoting hair growth, comprising the use of microneedles for the transplantation of cells and a method employing the use of same.


Grant
Agency: European Commission | Branch: H2020 | Program: SGA-RIA | Phase: FETFLAGSHIP | Award Amount: 89.00M | Year: 2016

Understanding the human brain is one of the greatest scientific challenges of our time. Such an understanding can provide profound insights into our humanity, leading to fundamentally new computing technologies, and transforming the diagnosis and treatment of brain disorders. Modern ICT brings this prospect within reach. The HBP Flagship Initiative (HBP) thus proposes a unique strategy that uses ICT to integrate neuroscience data from around the world, to develop a unified multi-level understanding of the brain and diseases, and ultimately to emulate its computational capabilities. The goal is to catalyze a global collaborative effort. During the HBPs first Specific Grant Agreement (SGA1), the HBP Core Project will outline the basis for building and operating a tightly integrated Research Infrastructure, providing HBP researchers and the scientific Community with unique resources and capabilities. Partnering Projects will enable independent research groups to expand the capabilities of the HBP Platforms, in order to use them to address otherwise intractable problems in neuroscience, computing and medicine in the future. In addition, collaborations with other national, European and international initiatives will create synergies, maximizing returns on research investment. SGA1 covers the detailed steps that will be taken to move the HBP closer to achieving its ambitious Flagship Objectives.


Grant
Agency: European Commission | Branch: H2020 | Program: RIA | Phase: EINFRA-22-2016 | Award Amount: 3.00M | Year: 2017

The goal of AARC2 is to design an AAI framework to develop interoperable AAI, to enable researchers to access the whole research and infrastructure service portfolio with one login. AARC2s objectives are: 1. enable federated access in research communities participating in AARC2 2. assist research communities to map their requirements to concrete service offerings 3. support research (e-)infrastructures to implement the integrated architecture and policies frameworks developed by AARC project 4. offer different trainings to adopt AARC/AARC2 results 5. enhance the integrated architecture AARC2 objectives will be achieved by: - Piloting selected research community use-cases (SA1) - Showcasing ready-to-use AAI solutions and pilot results to infrastructures (SA1-NA2) - Developing a virtual Competence Centre where infrastructure representatives and AARC2 team discuss AARC2 results deployment and approaches to use-cases (all WPs) - Promoting federated access and adoption of AARC2 results via training and outreach (NA2) - Expand support for new technologies and policies (JRA1 and NA3). - Follow a user-driven approach: development driven by use-cases and continuous community feedback on AARC2 work. Relevance to the work programme: - AARC2 will work with existing e-infrastructures and ESFRI projects to deploy and enhance (JRA1) the integrated AAI (built on eduIGAIN and federated access) delivered by AARC (obj1Development of a pan-European identity federation) - Use-cases that meet integration (accessing services offered by multiple e-infrastructures) and data-rich aspects included in AARC2 (SA1). AARC2 will work to enable federated access and to map the use-cases to existing AAI services and policy frameworks (obj2Stimulate AAI services supporting communities in the data-rich era) - AARC2 will liaise with security groups, NRENs and infrastructures to address best practices in cybersecurity and assurance (see NA3). (obj3Deliver an integrated infrastructure)


Hunter C.A.,University of Pennsylvania | Jones S.A.,University of Cardiff
Nature Immunology | Year: 2015

Interleukin 6 (IL-6) has a broad effect on cells of the immune system and those not of the immune system and often displays hormone-like characteristics that affect homeostatic processes. IL-6 has context-dependent pro- and anti-inflammatory properties and is now regarded as a prominent target for clinical intervention. However, the signaling cassette that controls the activity of IL-6 is complicated, and distinct intervention strategies can inhibit this pathway. Clinical experience with antagonists of IL-6 has raised new questions about how and when to block this cytokine to improve disease outcome and patient wellbeing. Here we discuss the effect of IL-6 on innate and adaptive immunity and the possible advantages of various antagonists of IL-6 and consider how the immunobiology of IL-6 may inform clinical decisions.


Owen M.J.,University of Cardiff
Neuron | Year: 2014

Recent findings in psychiatric genetics have crystallized concerns that diagnostic categories used in the clinic map poorly onto the underlying biology. If we are to harness developments in genetics and neuroscience to understand disease mechanisms and develop new treatments, we need new approaches to patient stratification that recognize the complexity and continuous nature of psychiatric traits and that are not constrained by current categorical approaches. Recognizing this, the National Institute for Mental Health (NIMH) has developed a novel framework to encourage more research of this kind. The implications of these recent findings and funding policy developments for neuroscience research are considerable. © 2014 Elsevier Inc.


Morgan B.P.,University of Cardiff
Acta neuropathologica communications | Year: 2014

INTRODUCTION: Inflammation and complement activation are firmly implicated in the pathology of multiple sclerosis; however, the extent and nature of their involvement in specific pathological processes such as axonal damage, myelin loss and disease progression remains uncertain. This study aims to bring clarity to these questions.RESULTS: We describe a detailed immunohistochemical study to localise a strategically selected set of complement proteins, activation products and regulators in brain and spinal cord tissue of 17 patients with progressive multiple sclerosis and 16 control donors, including 9 with central nervous system disease. Active, chronic active and chronic inactive multiple sclerosis plaques (35 in total) and non-plaque areas were examined.Multiple sclerosis plaques were consistently positive for complement proteins (C3, factor B, C1q), activation products (C3b, iC3b, C4d, terminal complement complex) and regulators (factor H, C1-inhibitor, clusterin), suggesting continuing local complement synthesis, activation and regulation despite the absence of other evidence of ongoing inflammation. Complement staining was most apparent in plaque and peri-plaque but also present in normal appearing white matter and cortical areas to a greater extent than in control tissue. C1q staining was present in all plaques suggesting a dominant role for the classical pathway. Cellular staining for complement components was largely restricted to reactive astrocytes, often adjacent to clusters of microglia in close apposition to complement opsonised myelin and damaged axons.CONCLUSIONS: The findings demonstrate the ubiquity of complement involvement in multiple sclerosis, suggest a pathogenic role for complement contributing to cell, axon and myelin damage and make the case for targeting complement for multiple sclerosis monitoring and therapy.


Better treatment is required for older patients with acute myeloid leukemia (AML) not considered fit for intensive chemotherapy. We report a randomized comparison of low-dose Ara-C (LDAC) vs the novel nucleoside, clofarabine, in untreated older patients with AML and high-risk myelodysplastic syndrome (MDS). A total of 406 patients with de novo (62%), secondary disease (24%), or high-risk MDS (>10% marrow blasts) (15%), median age 74 years, were randomized to LDAC 20 mg twice daily for 10 days every 6 weeks or clofarabine 20 mg/m(2) on days 1 to 5, both for up to 4 courses. These patients had more adverse demographics than contemporaneous intensively treated patients. The overall remission rate was 28%, and 2-year survival was 13%. Clofarabine significantly improved complete remission (22% vs 12%; hazard ratio [HR] = 0.47 [0.28-0.79]; P = .005) and overall response (38% vs 19%; HR = 0.41 [0.26-0.62]; P < .0001), but there was no difference in overall survival, explained by poorer survival in the clofarabine patients who did not gain complete remission and also following relapse. Clofarabine was more myelosuppressive and required more supportive care. Although clofarabine doubled remission rates, overall survival was not improved overall or in any subgroup. The treatment of patients of the type treated here remains a major unmet need.


Carpenter B.K.,University of Cardiff
Chemical Reviews | Year: 2013

Neglect of the excess internal energy, which all nascent reactive intermediates possess in some measure, can lead to serious misinterpretations of their behavior. Most thermal reactions of organic molecules are treated as if they occur on one PE surface, corresponding to the electronic ground states of all species involved. The implication of drawing a PE surface at all is that the Born-Oppenheimer approximation is valid everywhere, that is, that nuclear and electronic coordinates are always separable. However, once a reaction approaches a region on the groundstate PE surface corresponding to a reactive intermediate, this approximation might no longer be safe. In several instances the potential energy surfaces for reactions are actually simplified because ad hoc reaction pathways that may have been added to explain deviations from statistical behavior of reactive intermediates may no longer be necessary.

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