deletions | additions       diff --git a/urlstylerm___hyperse.tex b/urlstylerm___hyperse.tex  index 7929bb6..ab232af 100644  --- a/urlstylerm___hyperse.tex  +++ b/urlstylerm___hyperse.tex 
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Personalised medical treatment based on genome profiles is a major  goal of genetic research in the $21^{st}$ century  \cite[see][]{avery09,province08}. \citep[see][]{avery09,province08}.  However, complex genotype-environment interactions for common diseases make it  difficult to determine which specific genetic features should be used  to construct such profiles. Hence the prediction of genetic risk is a 
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shares with the more common Type 2 Diabetes mellitus (T2D) a  characteristic symptom of high blood glucose levels. In some cases,  this glucose also passes through to the urine, creating a sticky/sweet  substance that attracts ants \cite[see][pp. \citep[see][pp.  7,11]{ekoe02}. In T2D, this high blood glucose is caused by cells not responding to insulin  (insulin resistance), while in T1D the excess is caused by a reduction  in insulin production (insulin dependence). 
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manifest in childhood (younger than 18 years), and the disease is  believed to be caused by an abnormal immune response after exposure to  environmental triggers such as viruses, toxins or food  \cite[see][]{daneman06}. \citep[see][]{daneman06}.  \subsubsection{Symptoms, Diagnosis and Management of T1D}  \label{sec:sig-thy-t1d-symp-management} 
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distinct from T2D) encompasses a range of diseases that involve  autoimmunity. It can be diagnosed by the presence of antibodies to  glutamic acid decarboxylase, islet cells, insulin, or ICA512  \cite[see][p. \citep[see][p.  19]{ekoe02}. As the symptoms of T1D are caused by high blood glucose levels  (hyperglycaemia) due to a lack of insulin, these symptoms can be  relieved by the introduction of insulin into the blood. This is  typically carried out by supplying measured doses of insulin via  intramuscular injections or by the use of insulin pumps  \cite[see][]{daneman06}. \citep[see][]{daneman06}.  Individuals with T1D need a constant supply of insulin for survival, together with occasional insulin bursts to  control variable blood glucose levels throughout the day (e.g. after  meals). Individuals with T2D only require insulin for survival in rare  cases \cite[see][p. \citep[see][p.  16]{ekoe02}. Slow-release insulin and consumption of foods with a low glycaemic index can help to reduce the extremes of  T1D symptoms. 
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(hypoglycaemia), which produce short-term autonomic and neurological  problems such as trembling, dizziness, blurred vision, and difficulty  concentrating. Hypoglycaemia is treated either by ingestion of sugar,  or by intravenous glucose in severe cases \cite[see][]{daneman06}. \citep[see][]{daneman06}.  \subsubsection{Complications of T1D}  \label{sec:sig-thy-t1d-symptoms} 
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The initial symptoms of T1D are not usually severe, and the disease  may progress for a few years before a diagnosis is made and treatment  is given. However, long-term complications can appear when the disease  is not managed appropriately \cite[see][p. \citep[see][p.  8]{ekoe02}. Retinal damage progresses in about 20-25\% of individuals with T1D, with later stages  causing retinal detachment and consequent loss of sight. Renal failure  is also a problem in diabetic individuals, which is indicated by high 
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Neural defects are also a potential complication of T1D, most commonly  damage to peripheral nerves, leading to ulceration, poor healing and  gangrene unless good care is taken of the body extremities  \cite[see][]{daneman06}. \citep[see][]{daneman06}.  \subsubsection{Genetic Contribution to T1D Risk}  \label{sec:sig-thy-t1d-genetics} 
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susceptibility can be attributed to genetic factors. About 50\% of the  genetic contribution to T1D can be accounted for by variation in the  HLA region on chromosome 6, and 15\% is accounted for by variation in  two other genes, IDDM2 and IDDM12 \cite[see][]{daneman06}. \citep[]{daneman06}.  Incidence rates in migrant populations quickly converge to those of the  background population, suggesting that although the genetic  contribution to the disease is high, environmental factors probably  play a significant role in triggering the onset of disease  \cite[see][]{daneman06}. \citep[see][]{daneman06}.  \subsection{Wellcome Trust Case Control Consortium Study}  \label{sec:sig-thy-intr-wtccc} 
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region of chromosome 6, a region in which multiple SNPs had strong  associations with T1D, but only one of those SNPs (rs9272346) was  reported in the results table of the strongest associations  \cite[see][table \citep[see][table  3]{wellcome07}. \subsection{Replication Issues in GWAS}  \label{sec:sig-thy-intr-rep-iss} 
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followed up with studies attempting to determine the true causative  status of that association. Such causative studies are difficult, and  progress towards understanding the aetiology of common disease has  been slow \cite[see][]{dermitzakis09}. \citep[see][]{dermitzakis09}.  \subsection{Sampling Errors in GWAS}  \label{sec:sig-thy-intr-sampling} 
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exists. This is particularly important when considering populations  with mixed ancestry, where markers that are informative for  distinguishing population ancestry may become accidentally associated  with a particular disease \cite[see][]{pritchard01}. \citep[see][]{pritchard01}.  Bootstrapping by repeated re-sampling of a representative draw made  from a group can estimate population variation in genotype frequencies 
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method used in this chapter utilises a re-sampling technique in order  to reduce the influence of allele frequency variation in producing  false-positive results for particular samplings of the population.