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<title>The British Journal of Diabetes &amp; Vascular Disease</title>
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<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/5/197?rss=1">
<title><![CDATA[Influences of excess adiposity on reproductive function]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/5/197?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Mahmood, T. A]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:39:51 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409350280</dc:identifier>
<dc:title><![CDATA[Influences of excess adiposity on reproductive function]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>199</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>197</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/5/201?rss=1">
<title><![CDATA[Review: Diabetes and pregnancy: a review of pathology]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/5/201?rss=1</link>
<description><![CDATA[<p><b>Diabetes in pregnancy is associated with increased foetal morbidity and mortality. This article describes and reviews specific features of the placenta and the foetal anomalies seen in association with diabetes and briefly considers potential underlying mechanisms.</b></p>]]></description>
<dc:creator><![CDATA[Evans, M. J]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:40:40 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409344924</dc:identifier>
<dc:title><![CDATA[Review: Diabetes and pregnancy: a review of pathology]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>206</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>201</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/5/208?rss=1">
<title><![CDATA[Review: Diabetes in pregnancy: insulin resistance, obesity and placental dysfunction]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/5/208?rss=1</link>
<description><![CDATA[<p><b>Obesity in pregnancy is linked to increased morbidity and mortality for mother and baby. The incidence of gestational diabetes is increased approximately two to six-fold in women who are overweight-obese and the presence of diabetes is a further metabolic challenge which is associated with adverse outcomes. Herein the role of obesity is discussed in the generation of insulin resistance and inflammation and its contribution to placental dysfunction.</b></p>]]></description>
<dc:creator><![CDATA[Doshani, A., Konje, J. C]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:40:58 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409350273</dc:identifier>
<dc:title><![CDATA[Review: Diabetes in pregnancy: insulin resistance, obesity and placental dysfunction]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>212</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>208</prism:startingPage>
<prism:section>Articles</prism:section>
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<title><![CDATA[Review: Androgens, erectile dysfunction and cardiovascular risk in type 2 diabetes]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/5/214?rss=1</link>
<description><![CDATA[<p><b>Men with type 2 diabetes now require annual assessment for erectile dysfunction, and this should include assessment for testosterone deficiency. Up to 40% of patients might be candidates for testosterone replacement for the treatment of bothersome symptoms including erectile dysfunction, lethargy, fatigue, loss of libido and depressed mood. There is emerging evidence that there may also be benefits in the primary care quality parameters for type 2 diabetes.</b></p>]]></description>
<dc:creator><![CDATA[Hackett, G. I]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:41:04 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409340361</dc:identifier>
<dc:title><![CDATA[Review: Androgens, erectile dysfunction and cardiovascular risk in type 2 diabetes]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>217</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>214</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/5/220?rss=1">
<title><![CDATA[Metformin treatment for gestational diabetes]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/5/220?rss=1</link>
<description><![CDATA[<p><b>The prevalence of gestational diabetes mellitus (GDM) is rising as the pregnant population becomes older and more obese. This is concerning because GDM is associated with increased perinatal morbidity such as macrosomia and shoulder dystocia, and the need for instrumental delivery. In addition, the offspring of GDM women have increased long-term risks of obesity and type 2 diabetes. There is no doubt that treating women with GDM improves pregnancy outcomes. Conventionally this has been by diet and insulin. Although effective, insulin increases appetite leading to weight gain. It increases the risk of hypoglycaemia and needs to be given by injection. There is also a substantial cost in terms of time for teaching and educating patients. Metformin offers a logical alternative to insulin in GDM, by reducing insulin resistance. Recent trial evidence indicates it is safe and effective. We describe our experience with metformin in GDM and review the evidence.</b></p>]]></description>
<dc:creator><![CDATA[Hyer, S. L, Balani, J., Johnson, A., Shehata, H.]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:41:09 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409346767</dc:identifier>
<dc:title><![CDATA[Metformin treatment for gestational diabetes]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>225</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>220</prism:startingPage>
<prism:section>Articles</prism:section>
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<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/5/226?rss=1">
<title><![CDATA[Biochemical hypogonadism in men with type 2 diabetes in primary care practice]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/5/226?rss=1</link>
<description><![CDATA[<p>Objective:</p><p><b>This study explores the links between testosterone deficiency and Quality Outcomes Framework (QOF) parameters in three south Staffordshire practices prior to a major double-blind placebo-controlled intervention study.</b> Research design and methods:</p><p><b>Four hundred and eighty-eight consecutive type 2 diabetic patients, aged over 18, attending their general practitioner for routine diabetes visits were assessed for sex hormone binding globulin, total testosterone (TT), calculated free testosterone (FT) and bioavailable testosterone, glycated haemoglobin A1c (HbA1c), body mass index, waist circumference, blood pressure, lipid profile, Sexual Health Inventory for Men, and current and past prescriptions for erectile dysfunction (ED).</b></p><p>Results:</p><p><b>TT and FT were significantly inversely associated with raised body mass index, waist circumference and HbA1C. The prevalence of ED was 77%, which was associated with low levels of TT, FT and raised HbA1C. Only 10% were receiving treatment for ED.</b></p><p>Conclusions:</p><p><b>Patients with low testosterone were more likely to fall outside the QOF targets and new markers might be difficult to achieve unless low testosterone is addressed. There is a strong case for the inclusion of TT and FT estimation in routine diabetic care.</b></p>]]></description>
<dc:creator><![CDATA[Hackett, G. I, Cole, N. S, Deshpande, A. A, Popple, M. D, Kennedy, D., Wilkinson, P.]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:41:10 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409342635</dc:identifier>
<dc:title><![CDATA[Biochemical hypogonadism in men with type 2 diabetes in primary care practice]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>231</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>226</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/5/232?rss=1">
<title><![CDATA[Metformin: an important tool for endocrinology in the West Indies. New tricks for an old drug]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/5/232?rss=1</link>
<description><![CDATA[<p><b>Against the backdrop of an obesity pandemic, comes an increasing prevalence of metabolic (e.g. type 2 diabetes mellitus) and reproductive abnormalities (e.g. polycystic ovarian syndrome) mediated by the phenomenon of insulin resistance. Metformin is an inexpensive and widely available drug which partly through an insulin sensitising action has an antidiabetic action with unique cardioprotective effects and which has value in preventing progression of pre-diabetes to diabetes. Despite mounting favourable data its role in polycystic ovarian syndrome remains unsettled. The recent finding for its safety and efficacy in gestational diabetes, however, will no doubt lift concerns over its use in women in the reproductive age group. One immediate result would be its earlier and greater therapeutic application in under-resourced environments where cost and emotional barriers to insulin exist.</b></p>]]></description>
<dc:creator><![CDATA[Teelucksingh, S., Pinto Pereira, L. M]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:41:11 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409346766</dc:identifier>
<dc:title><![CDATA[Metformin: an important tool for endocrinology in the West Indies. New tricks for an old drug]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>236</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>232</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/5/237?rss=1">
<title><![CDATA[Male obesity: impact on fertility]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/5/237?rss=1</link>
<description><![CDATA[<p><b>Obesity has been shown to adversely affect male fertility, by reducing spermatogenesis. There are several aetiological theories including endocrine abnormalities, genetic, sexual dysfunction and testicular hyperthermia. Of these, endocrine abnormalities are likely to be the most important, involving increased oestrogen and increased insulin resistance, reduced androgens and reduced inhibin B levels. Possible management options include weight reduction by dieting or surgery and medical treatment to correct specific endocrine abnormalities, but as yet none has been proven to be effective.</b></p>]]></description>
<dc:creator><![CDATA[Kay, V. J, Barratt, C. L R]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:41:12 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409343132</dc:identifier>
<dc:title><![CDATA[Male obesity: impact on fertility]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>241</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>237</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/5/242?rss=1">
<title><![CDATA[The results of gastric bypass surgery in a teenager]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/5/242?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Teelucksingh, S., Dan, D.]]></dc:creator>
<dc:date>Wed, 21 Oct 2009 07:41:12 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409349969</dc:identifier>
<dc:title><![CDATA[The results of gastric bypass surgery in a teenager]]></dc:title>
<prism:number>5</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>243</prism:endingPage>
<prism:publicationDate>2009-09-01</prism:publicationDate>
<prism:startingPage>242</prism:startingPage>
<prism:section>Articles</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/4/142?rss=1">
<title><![CDATA[Diabetes -- from St Vincent to Glasgow. Have we progressed in 20 years?]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/4/142?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Felton, A.-M., Hall, M. S]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409341318</dc:identifier>
<dc:title><![CDATA[Diabetes -- from St Vincent to Glasgow. Have we progressed in 20 years?]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>144</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>142</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/4/147?rss=1">
<title><![CDATA[Diabetes medical treatment: not enough by far]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/4/147?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Wientjens, W. H.J.M.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409341771</dc:identifier>
<dc:title><![CDATA[Diabetes medical treatment: not enough by far]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>148</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>147</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/4/150?rss=1">
<title><![CDATA[Review: Adiponectin for prediction of cardiovascular risk?]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/4/150?rss=1</link>
<description><![CDATA[<p><b>Adiponectin is an endogenous insulin-sensitising and anti-inflammatory hormone, released by the adipose tissue. Because of its <I>in vitro</I> effects on endothelial cells, macrophages and vascular smooth muscle cells, adiponectin is thought to have anti-atherogenic properties. Moreover, findings from the Health Professionals Follow-up Studies and other cohort studies, mainly in male populations, suggest that adiponectin may be an independent predictor for cardiovascular risk. This, however, was not confirmed by subsequent studies that included female subjects, different ethnicities and patients with established coronary artery disease. The present article briefly summarises recent findings regarding the potential role of adiponectin as a predictor of risk and its biological role.</b></p><p><I>Br J Diabetes Vasc Dis</I> 2009;<b>9</b>: 150&mdash;154</p>]]></description>
<dc:creator><![CDATA[Karastergiou, K., Mohamed-Ali, V., Jahangiri, M., Kaski, J.-C.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409341326</dc:identifier>
<dc:title><![CDATA[Review: Adiponectin for prediction of cardiovascular risk?]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>154</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>150</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/4/155?rss=1">
<title><![CDATA[Review: The varied attractions of the diabetic foot]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/4/155?rss=1</link>
<description><![CDATA[<p><b>Various advances have been seen in the management of the diabetic foot. In some areas the rate of diabetes-related major amputations is declining. Duloxetine, pregabalin, venlafaxine and oxycodone are all well proven to help alleviate the pain of diabetic neuropathy. Negative pressure wound therapy has been shown to accelerate the healing of foot ulcers. New antibiotic policies designed to reduce <I>Clostridium difficile</I> and methicillin-resistant <I>Staphylococcus aureus</I> (MRSA) infections focus on narrow spectrum short duration antibiotics, and 80% of osteomyelitis can be successfully treated without surgery. Foot screening identifies patients who will ulcerate, with high-risk patients being up to 83 times more likely to ulcerate than low-risk patients. The &lsquo;holiday foot&rsquo; and distal peripheral vascular disease remain as major risk factors for foot ulcer development and non-healing. The diabetic foot provides many interesting and varied challenges for the interested clinician.</b></p><p><I>Br J Diabetes Vasc Dis</I> 2009;<b>9</b>:155&mdash;159</p>]]></description>
<dc:creator><![CDATA[Leese, G. P]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409341420</dc:identifier>
<dc:title><![CDATA[Review: The varied attractions of the diabetic foot]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>159</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>155</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/4/160?rss=1">
<title><![CDATA[Manifestation of lower extremity atherosclerosis in patients with high ankle-brachial index]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/4/160?rss=1</link>
<description><![CDATA[<p><b>The purpose of this study was to identify the manifestation of lower extremity atherosclerotic lesions in patients with high ankle-brachial index (ABI). We studied 92 diabetic patients at random from the Endocrine Department of the Chinese PLA General Hospital. According to the ABI value, the subjects were divided into three groups: high, normal and low ABI groups. On the basis of the results of lower extremity artery duplex ultrasound, the patients in the high ABI group had a lower incidence of low extremity artery occlusion than those in the low ABI group, and the atherosclerotic lesions of patients in the high group mainly displayed diffuse dot-like hyperechogenicity spots or small plaques (60.9%), and their atherosclerotic lesions in the lower extremity were mostly found in the distal segment (44.4%). This atherosclerosis in the lower extremities of patients in the high ABI group was shown to be consistent with the pathological features of artery intimal and medial calcification. It suggests that a high ABI is highly predictive of artery calcification, which is a marker of poor cardiovascular prognosis in diabetes.</b></p><p><I>Br J Diabetes Vasc Dis</I> 2009;<b>9</b>:160&mdash;164</p>]]></description>
<dc:creator><![CDATA[Hong Zhang,  , Li, X.-Y., Yajun Si,  , Xilie Lu,  , Liping Chen,  , Zhaoyang Liu,  ]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409342322</dc:identifier>
<dc:title><![CDATA[Manifestation of lower extremity atherosclerosis in patients with high ankle-brachial index]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>164</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>160</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/4/166?rss=1">
<title><![CDATA[High-mix analogue insulins: do they have a therapeutic role?]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/4/166?rss=1</link>
<description><![CDATA[<p>                 <b>It is estimated that 39% of diabetic patients worldwide that use insulin therapy                     are prescribed premixed insulin formulations, largely because of the practical                     advantages of addressing both prandial and basal insulin needs with a single                     product. High-mix insulin analogues are a relatively little used therapy and                     this paper explores their role in the management of diabetes. There is a paucity                     of research on their clinical efficacy and safety with regards to hypoglycaemia                     and we conclude that in certain patients they can be helpful for                     difficult-to-control postprandial hyperglycaemia, but there are no long-term                     outcome studies to assess whether this has an impact on cardiovascular outcomes                     and the current gold standard of insulin therapy still remains a basal bolus                     regimen.</b>             </p><p><I>Br J Diabetes Vasc Dis</I> 2009;<b>9</b>:166&mdash;170</p>]]></description>
<dc:creator><![CDATA[Grant, P., Dashora, U.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409340807</dc:identifier>
<dc:title><![CDATA[High-mix analogue insulins: do they have a therapeutic role?]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>170</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>166</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/4/171?rss=1">
<title><![CDATA[Cascade screening for familial hypercholesterolaemia and its effectiveness in the prevention of vascular disease]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/4/171?rss=1</link>
<description><![CDATA[<p><b>We describe cascade screening for familial hypercholesterolaemia (FH) and review the evidence for its effectiveness. We consider how it will be implemented into primary and secondary care, its potential advantages and disadvantages, and how it will help to prevent myocardial infarctions in patients with FH. Evidence from European countries and the recent pilot study in the UK show cascade screening for FH to be highly effective by facilitating early identification of many new patients. Treatment to lower cholesterol, if started early, is likely to lead to reductions in cardiovascular events. There are shortcomings in the current care of patients with FH and these should be addressed with the implementation of the new guidelines. To reduce the premature cardiovascular events seen in FH new healthcare infrastructures need to be in place and more education provided for both patients and professionals.</b></p><p><I>Br J Diabetes Vasc Dis</I> 2009;<b>9</b>:171&mdash;174</p>]]></description>
<dc:creator><![CDATA[Herman, K., Van Heyningen, C., Wile, D.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409339989</dc:identifier>
<dc:title><![CDATA[Cascade screening for familial hypercholesterolaemia and its effectiveness in the prevention of vascular disease]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>174</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>171</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/4/175?rss=1">
<title><![CDATA[Cardiovascular benefit of intensive glucose control: approaching closure]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/4/175?rss=1</link>
<description><![CDATA[<p><b>Several studies have demonstrated that lower blood glucose concentrations are associated with reduced cardiovascular endpoints. The publication of intervention trials designed to investigate the impact of tighter glycaemic control on cardiovascular morbidity and mortality in type 2 diabetes have generally failed, individually, to generate statistically significant improvements in cardiovascular endpoints. This has spurred controversy regarding the role of glycaemic control within a multifactorial approach to treatment. However, a recent meta-analysis of these intervention trials showed that intensive glucose control improves cardiovascular outcomes.</b></p>]]></description>
<dc:creator><![CDATA[Narendran, P.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409342641</dc:identifier>
<dc:title><![CDATA[Cardiovascular benefit of intensive glucose control: approaching closure]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>176</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>175</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/4/177?rss=1">
<title><![CDATA[Results of the LEAD-2 study in relation to NICE and ADA/EASD guidelines for         the treatment of type 2 diabetes in the UK]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/4/177?rss=1</link>
<description><![CDATA[<p>                 <b>Guidelines for the management of type 2 diabetes mellitus from the UK National                     Institute for Health and Clinical Excellence and the joint American Diabetes                     Association/European Association for the Study of Diabetes identify a role for                     glucagon-like peptide 1 (GLP-1) agonists as second- or third-line treatments. In                     the LEAD-2 trial the GLP-1 agonist liraglutide was similar to glimepiride for                     glycaemic control in patients receiving background metformin. Liraglutide was                     generally well tolerated, with a low incidence of hypoglycaemia, and it                     significantly reduced body weight and systolic blood pressure compared with                     glimepiride. These results suggest that addition of liraglutide may help to                     improve glycaemic control and reduce body weight and systolic blood pressure in                     patients with type 2 diabetes who have unsatisfactory control with metformin.                     Patients who are particularly obese or for whom hypoglycaemia is problematic may                     be especially suitable for this agent. The future place of liraglutide in                     guidelines will depend on further data regarding efficacy, tolerability and                     long-term benefits.</b>             </p>]]></description>
<dc:creator><![CDATA[Wilding, J.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409342637</dc:identifier>
<dc:title><![CDATA[Results of the LEAD-2 study in relation to NICE and ADA/EASD guidelines for         the treatment of type 2 diabetes in the UK]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>185</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>177</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/4/186?rss=1">
<title><![CDATA[Paradoxical fall in HDL cholesterol observed in a patient treated with rosiglitazone and pioglitazone]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/4/186?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Saraf, S., Nishtala, S., Parretti, H., Capps, N., Ramachandran, S.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409341325</dc:identifier>
<dc:title><![CDATA[Paradoxical fall in HDL cholesterol observed in a patient treated with rosiglitazone and pioglitazone]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>189</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>186</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/4/190?rss=1">
<title><![CDATA[An unusual diabetic foot collection]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/4/190?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Corfield, L., Sonnenberg, S., Bell, R.]]></dc:creator>
<dc:date>Fri, 28 Aug 2009 08:15:42 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409106477</dc:identifier>
<dc:title><![CDATA[An unusual diabetic foot collection]]></dc:title>
<prism:number>4</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>191</prism:endingPage>
<prism:publicationDate>2009-07-01</prism:publicationDate>
<prism:startingPage>190</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/3/96?rss=1">
<title><![CDATA[Diabetes P4P: a view from near and far]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/3/96?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Matfin, G.]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409105653</dc:identifier>
<dc:title><![CDATA[Diabetes P4P: a view from near and far]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>97</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>96</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/3/97?rss=1">
<title><![CDATA[Erratum]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/3/97?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/14746514090090030702</dc:identifier>
<dc:title><![CDATA[Erratum]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>97</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>97</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/3/99?rss=1">
<title><![CDATA[Review: Mechanisms of silent myocardial ischaemia: with particular reference to diabetes mellitus]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/3/99?rss=1</link>
<description><![CDATA[<p><b>Angina occurs relatively late following the onset of ischaemia: after the development of left ventricular dysfunction and electrocardiographic changes. Most ischaemic episodes are not severe enough or long enough to fully stimulate the anginal pain pathway. They are therefore clinically silent. More severe and prolonged episodes of ischaemia can also be silent. Pain thresholds vary between individuals and this is due to differences in gating mechanisms at the level of the thalamus. This gating appears to be modulated by levels of endogenous endorphins, among other mechanisms. This seems to have a relation to personality type. Silent ischemia is especially common in diabetic patients, and is often due to cardiac autonomic neuropathy.</b></p>]]></description>
<dc:creator><![CDATA[Dweck, M., Miller, D., Campbell, I. W, Francis, C M.]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409105371</dc:identifier>
<dc:title><![CDATA[Review: Mechanisms of silent myocardial ischaemia: with particular reference to diabetes mellitus]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>102</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>99</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/3/103?rss=1">
<title><![CDATA[Review: Bariatric surgery: to treat diabesity]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/3/103?rss=1</link>
<description><![CDATA[<p><b>In obese patients bariatric surgery is increasing in popularity as a strategy to promote, and maintain, weight loss. In obese type 2 diabetes bypass, bariatric surgery improves glycaemic control &mdash; often to a greater extent than would be anticipated by weight loss alone. Surgical bypass procedures appear to initially offer a greater glucose-lowering effect than surgical restriction procedures. This review considers the rationale for bariatric surgery as a treatment for diabesity and the implications of the different procedures on the secretion and action of enteral hormones.</b></p>]]></description>
<dc:creator><![CDATA[Flatt, P. R, Day, C., Bailey, C. J]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409103927</dc:identifier>
<dc:title><![CDATA[Review: Bariatric surgery: to treat diabesity]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>107</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>103</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/3/110?rss=1">
<title><![CDATA[Clinical aspects of silent myocardial ischaemia: with particular reference to diabetes mellitus]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/3/110?rss=1</link>
<description><![CDATA[<p><b>Silent ischaemia is a common, under-recognised condition that is associated with an adverse prognosis. It is a marker of significant underlying coronary artery disease and therefore of future cardiovascular events. It is more prevalent in the diabetic population and diagnosis is usually made by a positive exercise tolerance test, positive myocardial perfusion scan or stress echo. The basis of treatment, in diabetic and non-diabetic subjects, is risk factor modification and coronary revascularisation of prognostically important coronary disease. Diabetic patients should receive risk factor modification even in the absence of ischaemia. Detection of silent ischaemia allows patients with prognostically important disease to be offered further treatment. The difficulty lies in deciding who to investigate further for this surreptitious disorder. The following clinical markers are of predictive use in this regard: electrocardiographic changes; erectile dysfunction; peripheral vascular disease and cardiac autonomic neuropathy. Their presence should prompt further investigation for silent ischaemia. Conventional risk factors and breathlessness on exertion may also be helpful. We have proposed an algorithm for the detection, investigation and management of silent myocardial ischaemia in diabetic patients.</b></p>]]></description>
<dc:creator><![CDATA[Dweck, M., Campbell, I. W, Miller, D., Francis, C M.]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409105249</dc:identifier>
<dc:title><![CDATA[Clinical aspects of silent myocardial ischaemia: with particular reference to diabetes mellitus]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>116</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>110</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/3/119?rss=1">
<title><![CDATA[Diversity and complexity of urinary tract infection in diabetes mellitus]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/3/119?rss=1</link>
<description><![CDATA[<p><b>Urinary tract infections (UTIs) are a common burden in patients with diabetes mellitus. Cystitis, ascending infections leading to pyelonephritis, emphysematous complications and renal and perinephric abscesses are well recognised in this group of patients especially if glycaemic control is poor. Despite the clinical significance of UTI in diabetes, it is inadequately understood and management regimens are mostly not evidence based. Anticipation of potential complications and earlier interventions are vital to reduce serious adverse outcomes. Herein we discuss the aetiology, pathogenesis and management of UTI and its local and more remote complications.</b></p>]]></description>
<dc:creator><![CDATA[Hakeem, L. M, Bhattacharyya, D. N, Lafong, C., Janjua, K. S, Serhan, J. T, Campbell, I. W]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409105654</dc:identifier>
<dc:title><![CDATA[Diversity and complexity of urinary tract infection in diabetes mellitus]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>125</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>119</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/3/126?rss=1">
<title><![CDATA[Haemoglobin response to intravenous iron in non-dialysis patients with chronic kidney disease and diabetes]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/3/126?rss=1</link>
<description><![CDATA[<p><b>Aims. Our aim is to compare the response of people with or without diabetes to intravenous iron and to evaluate the efficacy of this therapy in improving haemoglobin (Hb) levels in non-dialysis patients according to chronic kidney disease (CKD) stage.</b></p><p><b>Method. This was a prospective study of 100 consecutive adult patients referred to the renal anaemia service for intravenous iron. Patients with other causes of anaemia or receiving erythropoietin therapy were excluded. Patients were given weekly intravenous doses of 200 mg iron sucrose for 4 weeks and monitored at weeks-1 and 5. Data, including diabetic/CKD status, were collated from patient records. Results. Pre-treatment Hb was similar in people with and without diabetes and treatment significantly increased Hb levels (0.5 g/dL, p&lt;0.003 and 0.5 g/dL, p&lt;0.0001 respectively). Pre-treatment transferrin saturation and the proportion of hypochromic red cells were not significantly different between the groups. Hb levels rose more in CKD stages 3 (0.5 g/dL, p&lt;0.05) and 4 (0.6 g/ dL, p&lt;0.02) than in stage 5 (-0.1 g/dL).</b></p><p><b>Conclusion. CKD patients with or without diabetes have similar iron status and Hb response to intravenous iron therapy. Patients with CKD stage 5 respond less well to intravenous iron than patients with CKD stages 3 or 4, despite having similar baseline iron status.</b></p>]]></description>
<dc:creator><![CDATA[Mostafa, S. A, Burden, A. C, Cropper, L., Tagboto, S.]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409105381</dc:identifier>
<dc:title><![CDATA[Haemoglobin response to intravenous iron in non-dialysis patients with chronic kidney disease and diabetes]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>128</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>126</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/3/129?rss=1">
<title><![CDATA[Diabetes treatments, gastrointestinal symptoms and lower gastrointestinal endoscopy]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/3/129?rss=1</link>
<description><![CDATA[<p><b>Background. Diabetes mellitus has been associated with an increased incidence of gastrointestinal (GI) symptoms, possibly related to diabetes medications.</b></p><p><b>Aims. The purpose of our study was to assess the prevalence of GI symptoms and pathology in diabetic subjects referred for lower GI endoscopy.</b></p><p><b>Results. We identified 31 diabetic patients from 621 patients undergoing lower GI endoscopy over a 6-month period. Diarrhoea and abdominal pain were common symptoms in the diabetic patients. Twelve diabetic subjects were investigated purely for GI symptoms and nine were referred with symptoms potentially related to diabetes medications. In these nine patients only one had an endoscopic diagnosis which accounted for their symptoms. Five patients had normal endoscopies. Conclusion. Diabetic medications may be associated with GI symptoms and alternative medications should be tried before referring for endoscopy.</b></p>]]></description>
<dc:creator><![CDATA[Kent, A. J, Graf, B., Prasad, P., Banks, M. R, Feher, M. D]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409104956</dc:identifier>
<dc:title><![CDATA[Diabetes treatments, gastrointestinal symptoms and lower gastrointestinal endoscopy]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>130</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>129</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/3/131?rss=1">
<title><![CDATA[Role of laparoscopic adjustable gastric banding in the treatment of obesity and related disorders]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/3/131?rss=1</link>
<description><![CDATA[<p><b>Bariatric surgery is increasing in popularity as an approach to the treatment of obesity, with a consequent benefit on co-morbid conditions. Laparoscopic gastric banding, as discussed herein, is a relatively safe, simple procedure in comparison with Roux-en-Y gastric bypass. The former technique offers comparable weight loss, but with some compromise on resolution of metabolic co-morbidities. The advantage, mainly relating to patient safety, makes laparosopic gastric banding an effective option for any obese individual in whom weight loss surgery is indicated.</b></p>]]></description>
<dc:creator><![CDATA[Singhal, R., Super, P.]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409105846</dc:identifier>
<dc:title><![CDATA[Role of laparoscopic adjustable gastric banding in the treatment of obesity and related disorders]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>133</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>131</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/3/134?rss=1">
<title><![CDATA[HbA1c - changing units]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/3/134?rss=1</link>
<description><![CDATA[<p><b>Measurement of glycated haemoglobin A<SUB>1C</SUB> (HbA<SUB>1C</SUB>) provides an indication of longer-term glycaemic control. Standardisation of this test between laboratories is difficult to achieve, and most assays are currently calibrated to the values used in the Diabetes Control and Complications Trial (DCCT-aligned). With the availability of more specific reference standards it is now proposed that HbA<SUB>1C</SUB> is expressed as mmol HbA<SUB>1C</SUB> per mol of non-glycated haemoglobin. An HbA<SUB>1C</SUB> of 7% is approximately equal to 53 mmol/mol.</b></p>]]></description>
<dc:creator><![CDATA[Day, C., Bailey, C. J]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409106110</dc:identifier>
<dc:title><![CDATA[HbA1c - changing units]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>136</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>134</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/3/137?rss=1">
<title><![CDATA[Early-onset type 2 diabetes: not a benign condition]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/3/137?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Song, S. H]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409103561</dc:identifier>
<dc:title><![CDATA[Early-onset type 2 diabetes: not a benign condition]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>138</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>137</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/3/139?rss=1">
<title><![CDATA[Highlights from the Fifth International Symposium on Diabetes and Pregnancy]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/3/139?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Duncan, C.]]></dc:creator>
<dc:date>Mon, 08 Jun 2009 08:17:02 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409106324</dc:identifier>
<dc:title><![CDATA[Highlights from the Fifth International Symposium on Diabetes and Pregnancy]]></dc:title>
<prism:number>3</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>140</prism:endingPage>
<prism:publicationDate>2009-05-01</prism:publicationDate>
<prism:startingPage>139</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/2/43?rss=1">
<title><![CDATA[Editorial: Which weight loss diet?]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/2/43?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Day, C., Bailey, C. J]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409106083</dc:identifier>
<dc:title><![CDATA[Editorial: Which weight loss diet?]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>43</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>43</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/2/44?rss=1">
<title><![CDATA[Review: Maximising the therapeutic potential of glucagon-like peptide-1 in type 2 diabetes]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/2/44?rss=1</link>
<description><![CDATA[<p><b>Tight control of blood glucose levels is fundamental for delaying or preventing the progression of metabolic complications in type 2 diabetes. Glucagon-like peptide-1 (GLP-1), secreted from the L-cells of the distal small intestine and colon in response to feeding, promotes insulin production and secretion, reduces glucagon secretion, delays gastric emptying and induces satiety. However, native GLP-1 is rapidly degraded by dipeptidyl peptidase (DPP) 4 reducing its therapeutic utility. Two approaches have been adopted to extend duration of action, namely enzyme-resistant GLP-1 mimetics and DPP 4 inhibitors which additionally promote insulin release by GIP. Clinical trials of incretin-based therapies have shown good efficacy in improving glycaemic control in type 2 diabetes. These therapies can be added to metformin or thiazolidinediones in order to target efects of insulin secretion as well as insulin action. However, incretin therapies also show potential when combined with approaches that increase insulin by endogenous (via sulphonylureas) or exogenous routes. Synergistic actions of incretin therapies with sulphonylureas on pancreatic beta-cells are also potentially advantageous. Incretin therapies can reduce hypoglycaemia since GLP-1 increases glucose sensing of both insulin and glucagon-secreting cells.</b> <I>Br J Diabetes Vasc Dis</I> 2009; <b>9</b>: 44&mdash;52</p>]]></description>
<dc:creator><![CDATA[Irwin, N., Moodley, M., Flatt, P. R]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651408101961</dc:identifier>
<dc:title><![CDATA[Review: Maximising the therapeutic potential of glucagon-like peptide-1 in type 2 diabetes]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>52</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>44</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/2/53?rss=1">
<title><![CDATA[Review: Durable glycaemia -- the promised land]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/2/53?rss=1</link>
<description><![CDATA[<p><b>Patients with type 2 diabetes experience progressive loss of glycaemic control and require intensification of glucose-lowering therapies. Durable glycaemic control has been shown to reduce microvascular and macrovascular complications in patients with type 1 diabetes or type 2 diabetes. The range of available glucose-lowering agents has been expanded with the addition of the thiazolidinediones (TZDs) pioglitazone androsiglitazone and, more recently, dipeptidyl peptidase-4 inhibitors and the glucagon-like peptide-1 analogue exenatide. In clinical trials, the TZDs have provided sustained glycaemic control, both in monotherapy and in combination with metformin and sulphonylureas. Pioglitazone has also been associated with improvements in the long-term cardiovascular morbidity and mortality of patients with type 2 diabetes.</b> <I>Br J Diabetes Vasc Dis</I> 2009;<b>9</b>:53&mdash;63</p>]]></description>
<dc:creator><![CDATA[Campbell, I. W]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651408100470</dc:identifier>
<dc:title><![CDATA[Review: Durable glycaemia -- the promised land]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>63</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>53</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/2/65?rss=1">
<title><![CDATA[Increased arterial stiffness in normoglycaemic offspring of newly diagnosed, never treated type 2 diabetic and impaired glucose tolerance parents]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/2/65?rss=1</link>
<description><![CDATA[<p><b>Arterial stiffness has been used to demonstrate vasculopathy in adults with diabetes but studies on arterial stiffness in offspring of diabetic patients are scarce, and no study has been reported in the offspring of parents with impaired glucose tolerance (IGT). In this study arterial stiffness in normoglycaemic offspring (n</b>=<b>30) of parents with type 2 diabetes, normoglycaemic offspring (n</b> =<b>30) of IGT parents and 30 age and sex-matched normoglycaemic offspring of normoglycaemic parents was investigated. Arterial stiffness was assessed by pulse wave velocity (PWV) and augmentation index (AI) using SphygmoCor. Significantly higher PWV was noted in offspring of type 2 diabetes than in offspring of normoglycaemic parents (6.94&plusmn;0.9 vs. 6.33&plusmn;0.7 m/s, p</b>=<b> 0.010). Offspring of type 2 diabetes parents also demonstrated significantly higher PWV than IGT offspring (6.94&plusmn;0.9 vs. 6.43&plusmn;1.1, p</b>=<b>0.021). Significantly higher AI was observed in offspring of type 2 diabetes and IGT parents than progeny of normoglycaemic parents (105.62&plusmn;14.2 vs. 96.42&plusmn;7.7, p</b>=<b>0.001; 104.98&plusmn;11.1 vs. 96.42&plusmn;7.7%, p</b>=<b>0.004, espectively). The study demonstrated that normoglycaemic offspring of newly diagnosed, never treated type 2 diabetes and IGT parents had increased arterial stiffness. Such increases in arterial stiffness revealed early manifestations of preclinical vasculopathy and potentially increased risk for development of macrovascular diseases in the normoglycaemic offspring.</b> <I>Br J Diabetes Vasc Dis</I> 2009;<b>9:</b> 65&mdash;68.</p>]]></description>
<dc:creator><![CDATA[Rahman, S., Aziz Al-Safi Ismail,  , Shaiful Bahari Ismail,  , Nyi Nyi Naing,  , Abdul Rashid Abdul Rahman,  ]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409102801</dc:identifier>
<dc:title><![CDATA[Increased arterial stiffness in normoglycaemic offspring of newly diagnosed, never treated type 2 diabetic and impaired glucose tolerance parents]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>68</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>65</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/2/69?rss=1">
<title><![CDATA[Management of type 2 diabetes and lipids: a critique of the NICE guidelines 2008]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/2/69?rss=1</link>
<description><![CDATA[<p><b>Type 2 diabetes and cardiovascular disease are leading causes of morbidity and mortality in the UK. Appropriate and effective management of these conditions and associated risk factors such as hyperlipidaemia are the cornerstones to improving general well being and health outcomes. In 2008, the National Institute for Health and Clinical Excellence (NICE) published guidelines on the management of type 2 diabetes (CG66) and lipid modification (CG67). This article aims to give a practical critique of the clinical management strategies recommended by these guidelines.</b> <I>Br J Diabetes vasc Dis 2009;</I><b>9:</b>69&mdash;74</p>]]></description>
<dc:creator><![CDATA[Song, S. H, Gray, T. A]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409103867</dc:identifier>
<dc:title><![CDATA[Management of type 2 diabetes and lipids: a critique of the NICE guidelines 2008]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>74</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>69</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/2/75?rss=1">
<title><![CDATA[Haemorrhagic bullous Streptococcus pneumoniae cellulitis in type 2 diabetes mellitus]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/2/75?rss=1</link>
<description><![CDATA[<p><b>Although <I>Streptococcus pneumoniae</I> is the most common cause of community-acquired bacterial pneumonia, its involvement in skin infection is notably infrequent. Typically, patients with pneumococcal cellulitis have a background of alcohol abuse, diabetes or immunosuppression due to an underlying chronic illness. In contrast to other common bacterial infections patients often require surgical interventions and prolonged hospitalisations due to tissue necrosis, suppurative complications and bacteraemia. Early recognition and aggressive management is vital in reducing morbidity and mortality. We describe a case of a diabetic patient who presented with haemorrhagic bullous pneumococcal cellulitis and required vascular surgical intervention due to peripheral vascular disease and extensive tissue necrosis.</b> <I>Br J Diabetes Vasc Dis 2008;</I><b>8</b>:75&mdash;79</p>]]></description>
<dc:creator><![CDATA[Hakeem, L. M, Urolagin, M., Bhattacharyya, D. N, Campbell, I. W, Griffiths, G.]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651408100353</dc:identifier>
<dc:title><![CDATA[Haemorrhagic bullous Streptococcus pneumoniae cellulitis in type 2 diabetes mellitus]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>79</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>75</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/2/81?rss=1">
<title><![CDATA[Prevalence of HTLV-1 infection in type 2 diabetic patients in Mashhad, northeastern Iran]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/2/81?rss=1</link>
<description><![CDATA[<p>Objective <b>The aim of this study was to evaluate the prevalence of human T cell leukaemia virus type 1 (HTLV-1) infection among patients with type 2 diabetes mellitus in Mashhad in northeastern Iran.</b></p><p>Methods <b>A total of 266 consecutive type 2 diabetic patients (mean age 54.36&plusmn;11.58 years) attending our unit were compared with 60,892 non-diabetic blood donors for the presence of HTLV-1 infection. Serological testing for HTLV-1 was undertaken using an enzyme-linked immunosorbent assay, and a polymerase chain reaction (PCR) was performed in positive HTLV-1 samples.</b></p><p>Results <b>PCR confirmed HTLV-1 infection in ten patients. The prevalence of HTLV-1 infection was more than five-fold higher in the diabetic patients than the blood donor group (3.75 vs. 0.663%; p</b>&lt;<b>0.001). There was no apparent association between HTLV-1 infection and age, sex, body mass index, diabetes duration or glycaemic control.</b></p><p>Conclusions <b>A higher prevalence of HTLV-1 infection was detected in diabetic patients and this should be borne in mind when treating type 2 diabetic patients in regions where HTLV-1 infection is endemic.</b> <I>Br J Diabetes Vasc Dis 2009;</I><b> 9:</b>81&mdash;83</p>]]></description>
<dc:creator><![CDATA[Taghavi, M., Fatemi, S.]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409103583</dc:identifier>
<dc:title><![CDATA[Prevalence of HTLV-1 infection in type 2 diabetic patients in Mashhad, northeastern Iran]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>83</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>81</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/content/abstract/9/2/84?rss=1">
<title><![CDATA[Prescribing errors in diabetes]]></title>
<link>http://dvd.sagepub.com/cgi/content/abstract/9/2/84?rss=1</link>
<description><![CDATA[<p><b>Prescribing errors in diabetes have the potential to cause serious adverse effects. Antidiabetic agents are a significant cause of admission to hospital. Prescribing errors can be caused by poor handwriting, failure to communicate clearly, and by the use of inappropriate abbreviations. Serious errors involving insulin have been reported in the UK media. While education and training may reduce the number of errors, experience shows that errors will continue to occur without changes to systems.</b> <I>Br J Diabetes Vasc Dis 2009;</I><b>9:</b>84&mdash;88</p>]]></description>
<dc:creator><![CDATA[Cox, A. R, Ferner, R. E]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409103902</dc:identifier>
<dc:title><![CDATA[Prescribing errors in diabetes]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>88</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>84</prism:startingPage>
<prism:section>Article</prism:section>
</item>

<item rdf:about="http://dvd.sagepub.com/cgi/reprint/9/2/90?rss=1">
<title><![CDATA[Phaeochromocytoma diagnosed at cardiac catheterisation]]></title>
<link>http://dvd.sagepub.com/cgi/reprint/9/2/90?rss=1</link>
<description><![CDATA[]]></description>
<dc:creator><![CDATA[Lulsegged, A., Quin, J., Holmberg, S., Ghuran, A.]]></dc:creator>
<dc:date>Tue, 14 Apr 2009 04:36:41 PDT</dc:date>
<dc:identifier>info:doi/10.1177/1474651409103560</dc:identifier>
<dc:title><![CDATA[Phaeochromocytoma diagnosed at cardiac catheterisation]]></dc:title>
<prism:number>2</prism:number>
<prism:volume>9</prism:volume>
<prism:endingPage>91</prism:endingPage>
<prism:publicationDate>2009-03-01</prism:publicationDate>
<prism:startingPage>90</prism:startingPage>
<prism:section>Article</prism:section>
</item>

</rdf:RDF>