winners of the Nobel Prize for Physiology or Medicine worked or were educated at Oxford, and the division is home to 29 Fellows of the Royal Society and 68 Fellows of the Academy of Medical Sciences. Now we can control both the phase lines connected to the two terminals of the SPDT switches using master switches MS1 and MS2.

It is one of the largest biomedical research centres in Europe, with over 2,500 people involved in research and more than 2,800 students, and brings in around two-thirds of Oxford University’s external research income. Listed by itself, that would make it the fifth largest university in the UK in terms of research grants and contracts. Published online on 15 May 2011 in Nature Genetics, the study was one part of a large multi-national collaboration funded by the Wellcome Trust, known as the MuTHER study. It involves researchers from King’s College London, University of Oxford, The Wellcome Trust Sanger Institute, and the University of Geneva. DeCODE Genetics also contributed to the results reported in this paper. King’s College London and Guy’s and St Thomas’, King’s College Hospital and South London and Maudsley NHS Foundation Trusts are part of King’s Health Partners. King’s Health Partners Academic Health Sciences Centre (AHSC) is a pioneering global collaboration between one of the world’s leading research-led universities and three of London’s most successful NHS Foundation Trusts, including leading teaching hospitals and comprehensive mental health services. KLF14 seems to act as a master switch controlling processes that connect changes in the behaviour of subcutaneous fat to disturbances in muscle and liver that contribute to diabetes and other conditions. We are working hard right now to understand these processes and how we can use this information to improve treatment of these conditions.”KLF14 is a master regulator of gene expression in adipose tissue. p-value distribution of association between the KLF14 cis-eQTL rs4731702 and expression levels of ~24,000 probes in adipose tissue. Enrichment for low p-values suggests that KLF14 is a master-regulator of gene expression in adipose tissue. In many ways, The Master Switch fills a valuable niche in the literature on communication‐information policy. No other book that I know of takes us so effortlessly through 150 years of change and equilibrium in the telecommunication, media and information industries with an eye for the entertaining anecdote and the enlivening detail. But the book is also a big disappointment. Ultimately, it fails to deliver conceptual and analytical insights commensurate with its grand scope. This failure does not become fully apparent until the last chapter, which makes the letdown all the more jarring.

Consider the master switch is OFF (MS1 – OFF), in this condition only one terminal of the SPDT switches has the phase line, and all the terminals connected to the master switch remain open. So only switches positioned to the live terminal (connected to direct phase line) will ON the lamp, where switches positioned to open terminal OFF the lamp. So, the switch S1, S2, S3, and S4 can individually control lamps L1, L2, L3, and L4 respectively. The Isolator can be controlled by any number of switches although the usual configuration is one internal on- off switch and one external kill button. However, our system also allows multiple kill switches to be installed and the fitment of two external ‘kill’ buttons, one on each side of a race car, has become popular safety feature. As the amount and distribution of fat plays a key role in susceptibility to metabolic diseases such as obesity, heart disease and diabetes, this study highlights the regulatory gene as a possible target for future treatments to fight these diseases.

A major strength of Oxford medicine is its long-standing network of clinical research units in Asia and Africa, enabling world-leading research on the most pressing global health challenges such as malaria, TB, HIV/AIDS and flu. Oxford is also renowned for its large-scale studies into the causes and treatment of cancer, heart disease, diabetes and other common conditions. The researchers examined over 20,000 genes in subcutaneous fat biopsies from 800 UK female twin volunteers. They found an association between the KLF14 gene and the expression levels of multiple distant genes found in fat tissue, which means it acts as a master switch to control these genes. This was then confirmed in a further independent sample of 600 subcutaneous fat biopsies from Icelandic subjects.

This circuit is the same as the master ON circuit the only change is an additional Master switch (MS2) which is added to the phase line that was previously connected directly to the terminals of switches S1 to S4. It was already known that the KLF14 gene is linked to type 2 diabetes and cholesterol levels but, until now, how it did this and the role it played in controlling other genes located further away on the genome was unknown. Features a manual bypass that enables even non-technical staff to easily switch between 2 independent power sources in the event of a supply failure. This is the first major study that shows how small changes in one master regulator gene can cause a cascade of other metabolic effects in other genes. This has great therapeutic potential particularly as by studying large detailed populations such as the twins we hope to find more of these regulators.” These other genes found to be controlled by KLF14 are in fact linked to a range of metabolic traits Including body-mass index (obesity), cholesterol, insulin and glucose levels, highlighting the interconnectedness of metabolic traits.

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A team of researchers, led by King’s College London and the University of Oxford, have found that a gene linked to type 2 diabetes and cholesterol levels is in fact a ‘master regulator’ gene, which controls the behaviour of other genes found within fat tissues in the body. Oxford University’s Medical Sciences Division is recognized internationally for its outstanding research and teaching, attracting the brightest minds from all over the world.