- Total grants
- Total funders
- Total recipients
- Earliest award date
- 09 Jun 1998
- Latest award date
- 05 May 2020
- Total GBP grants
- Total GBP awarded
- Largest GBP award
- Smallest GBP award
- Total Non-GBP grants
Vacation Scholarships 2018 - Queen Mary University of London
Vacation Scholarships 2017- Queen Mary University London
The purpose of this research is to conduct a wide ranging investigation into sleep disorders in early modern society, and their implications for a number of other areas of research. Firstly, I will look at the definitions, and theories of causes and cures, in early modern medical texts, physicians' casebooks, treatises on the supernatural, legal texts and popular printed ballads, in order to ascertain how far sleep disorders were perceived to be a natural or supernatural problem. I will then c ompare this to the findings of recent research into sleep disorders in order to discover what areas remain unexplained by modern science, and whether modern clinical research can help us to explain witchcraft accusations in the past. A second goal will be to find out what impact medical theory had on domestic medicine. The main sources for this will be receipt books and diaries. The third aim of this project will be to understand sleep from the point of view of practical divinity. I will ex amine sections on sleep in sermons and religious treatises, looking in particular at the relationship between sin, guilt and troubled sleep.
The goal of this proposal is to evaluate the impact of cotrimoxazole, integrated with a package of nutrition interventions early in the lifecourse, on healthy birth and growth in rural Zimbabwe. Stunting is highly prevalent, begins in utero and causes increased mortality and reduced long-term productivity. Current nutrition-specific interventions have only a marginal impact. New approaches targeting mechanistic pathways early in the life-cycle are needed. We will use cotrimoxazole to test the hy pothesis that inflammation is a common mechanism underlying preterm birth, intrauterine growth restriction and postnatal stunting. We hypothesize that inflammation is driven predominantly by clinical and subclinical infections, abnormal micobiota composition and environmental enteric dysfunction, all of which will be impacted by cotrimoxazole. The specific questions are: 1) Does antenatal cotrimoxazole improve fetal growth and reduce prematurity? 2) Does postnatal cotrimoxazole improve li near growth? 3) Through what mechanistic pathways does cotrimoxazole operate? We will conduct a randomised clinical trial of cotrimoxazole, integrated with a package of evidence-based nutrition interventions, in two phases. First, women will receive a lipid-based nutrient supplement (LiNS) and nutrition education during pregnancy and will be randomised to daily cotrimoxazole or placebo, with a primary outcome of birth weight. Second, breastfeeding women will continue to receive LiNS and nut rition education; their infants will be randomised to daily cotrimoxazole or placebo, with a primary outcome of height-for-age Z-score at 6 months. Finally, we will investigate the impact of cotrimoxazole on underlying biological pathways to better understand its mechanism of action.
Genetic, Biochemical and Functional Analyses of Genes in the Highly Atherogenic Disorder Familial Combined Hyperlipidemia (FCHL). 27 Jun 2012
Background: Genetic hyperlipidemias are a common cause of premature coronary heart disease. Familial Combined Hyperlipidemia(FCHL) is a prevalent form of inherited hyperlipidemia. Elucidating the aetiologies of FCHL have been difficult because the condition is genetically heterogeneous, and common variants that raise blood lipid levels in the general population have almost no effect in this disorder(s). FCHL is likely to run in families because causative lesions have a moderate-to-large impact o n lipid levels. Aims: The aim of my Fellowship is to acquire data that will ultimately lead to genetic (and definitive) diagnosis of FCHL (and reduce its clinical consequences), similar to that implemented for monogenic Familial Hypercholesterolemia. Methods: By considering very recent genetic and biological data, I have started screening the largest assembled cohort of FCHL families worldwide for deleterious lesions in three 'new' genes. I am continuing my in-depth sequence analyses in f urther patients, and will undertake cell-based studies to determine the relationships between gene variants/mutations, impaired protein function(s) and FCHL-lipid abnormalities. Scientific and Medical Opportunities: These include understanding the mechanistic and biochemical processes regulating blood lipid levels. Identifying the aetiologies of FCHL will lead to development of targeted and effective therapeutic options, thereby reducing associated cardiovascular manifestations.
"The pathology museum seminar series" to be held at St Bartholomew's pathology museum from October 2011 to May 2012 17 Oct 2011