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	<title>Brisbane Podiatry</title>
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	<link>http://www.brisbanepodiatry.net.au</link>
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		<title>ankle; +56 new citations</title>
		<link>http://www.brisbanepodiatry.net.au/2013/ankle-56-new-citations/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/ankle-56-new-citations/#comments</comments>
		<pubDate>Wed, 19 Jun 2013 13:54:41 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Podiatry]]></category>
		<category><![CDATA[Ankle]]></category>
		<category><![CDATA[citations]]></category>

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		<description><![CDATA[56 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: ankle These pubmed results were generated on 2013/06/19 PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950&#8242;s. These citations are from MEDLINE [...]]]></description>
			<content:encoded><![CDATA[<p>56 new pubmed citations were retrieved for your search.<br />
Click on the search hyperlink below to display the complete search results:
</p>
<p align="center"><b>ankle</b></p>
<p>These pubmed results were generated on 2013/06/19</p>
<p>PubMed, a service of the National Library of Medicine, includes over 15 million<br />
citations for biomedical articles back to the 1950&#8242;s.<br />
These citations are from MEDLINE and additional life science journals.<br />
PubMed includes links to many sites providing full text articles and other related resources.</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Search&#038;db=pubmed&#038;term=(((ankle)%20AND%20%222013%2F06%2F15%2009.55%22%5BMHDA%5D%3A%222013%2F06%2F19%2009.54%22%5BMHDA%5D))%20NOT%20((%20(((%22ankle%22%5BTIAB%5D%20OR%20%22ankle%22%5BTIAB%5D%20OR%20%22ankle%20joint%22%5BTIAB%5D%20OR%20(%22ankle%22%5BTIAB%5D%20AND%20%22joint%22%5BTIAB%5D)%20OR%20%22ankle%20joint%22%5BTIAB%5D)))%20AND%20%220001%22%5BEDAT%5D%3A%222013%2F06%2F15%2009.55%22%5BEDAT%5D))">pubmed: ankle</a></p>
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		<title>foot; +83 new citations</title>
		<link>http://www.brisbanepodiatry.net.au/2013/foot-83-new-citations/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/foot-83-new-citations/#comments</comments>
		<pubDate>Wed, 19 Jun 2013 10:54:46 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Podiatry]]></category>
		<category><![CDATA[citations]]></category>
		<category><![CDATA[Foot]]></category>

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		<description><![CDATA[83 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: foot These pubmed results were generated on 2013/06/19 PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950&#8242;s. These citations are from MEDLINE [...]]]></description>
			<content:encoded><![CDATA[<p>83 new pubmed citations were retrieved for your search.<br />
Click on the search hyperlink below to display the complete search results:
</p>
<p align="center"><b>foot</b></p>
<p>These pubmed results were generated on 2013/06/19</p>
<p>PubMed, a service of the National Library of Medicine, includes over 15 million<br />
citations for biomedical articles back to the 1950&#8242;s.<br />
These citations are from MEDLINE and additional life science journals.<br />
PubMed includes links to many sites providing full text articles and other related resources.</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/sites/entrez?cmd=Search&#038;db=pubmed&#038;term=(((foot)%20AND%20%222013%2F06%2F16%2006.55%22%5BMHDA%5D%3A%222013%2F06%2F19%2006.54%22%5BMHDA%5D))%20NOT%20((%20(((%22foot%22%5BTIAB%5D%20OR%20%22foot%22%5BTIAB%5D)))%20AND%20%220001%22%5BEDAT%5D%3A%222013%2F06%2F16%2006.55%22%5BEDAT%5D))">pubmed: foot</a></p>
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		<item>
		<title>Accumulation of non-compressive fascicular lesions underlies NF2 polyneuropathy.</title>
		<link>http://www.brisbanepodiatry.net.au/2013/accumulation-of-non-compressive-fascicular-lesions-underlies-nf2-polyneuropathy/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/accumulation-of-non-compressive-fascicular-lesions-underlies-nf2-polyneuropathy/#comments</comments>
		<pubDate>Mon, 17 Jun 2013 10:54:36 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Podiatry]]></category>
		<category><![CDATA[accumulation]]></category>
		<category><![CDATA[fascicular]]></category>
		<category><![CDATA[Lesions.]]></category>
		<category><![CDATA[noncompressive]]></category>
		<category><![CDATA[polyneuropathy]]></category>
		<category><![CDATA[underlies]]></category>

		<guid isPermaLink="false">http://www.brisbanepodiatry.net.au/2013/accumulation-of-non-compressive-fascicular-lesions-underlies-nf2-polyneuropathy/</guid>
		<description><![CDATA[Related Articles Accumulation of non-compressive fascicular lesions underlies NF2 polyneuropathy. J Neurol. 2013 Jan;260(1):38-46 Authors: Bäumer P, Mautner VF, Bäumer T, Schuhmann MU, Tatagiba M, Heiland S, Kaestel T, Bendszus M, Pham M Abstract A distinct polyneuropathy (PNP) syndrome affects up to 66 % of patients with neurofibromatosis II (NF2). Whether this is primarily a [...]]]></description>
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<td align="left"><img src="//www.ncbi.nlm.nih.gov/corehtml/query/egifs/http:--production.springer.de-OnlineResources-Logos-springerlink.gif" border="0"/> </td>
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</tr>
</table>
<p><b>Accumulation of non-compressive fascicular lesions underlies NF2 polyneuropathy.</b></p>
<p>J Neurol. 2013 Jan;260(1):38-46</p>
<p>Authors:  Bäumer P, Mautner VF, Bäumer T, Schuhmann MU, Tatagiba M, Heiland S, Kaestel T, Bendszus M, Pham M</p>
<p>Abstract<br/><br />
        A distinct polyneuropathy (PNP) syndrome affects up to 66 % of patients with neurofibromatosis II (NF2). Whether this is primarily a diffuse PNP or due to single, surgically amenable mass lesions has not yet been conclusively demonstrated. We aimed to solve this question by investigating the pathomorphological MR imaging correlate of this rare disorder. Eight patients with NF2-PNP were characterized by clinical examination, electrophysiological studies, and genetic analysis. All patients additionally underwent extended peripheral nerve imaging by a novel protocol of large-coverage high-resolution MRI. Quantitative analyses were performed by separately evaluating cross-sectional images, and by categorizing lesions into non-compressive fascicular microlesions (&lt;2 mm), intermediate lesions (2-5 mm), and compressive macrolesions (&gt;5 mm). The predominant imaging findings were non-compressive fascicular microlesions and intermediate lesions. Proximal-to-distal cumulative lesion burden of these lesions correlated strongly with the severity of clinical symptoms of NF2-PNP. In contrast, compressive macrolesions were not found at all in several symptomatic extremities. We conclude that proximal-to-distal accumulation of non-compressive fascicular lesions instead of compressive mass lesions predominantly underlies the clinical manifestation and severity of NF2-associated PNP. Diagnostic management may now be assisted by large-coverage high-resolution imaging of plexus and peripheral nerves. Additionally, the results underscore the feasibility of this new method, which may open up new diagnostic and investigative possibilities for other disseminated disorders of the peripheral nervous system.<br/>
        </p>
<p>PMID: 22760943 [PubMed - indexed for MEDLINE]</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/pubmed/22760943?dopt=Abstract">pubmed: ankle</a></p>
]]></content:encoded>
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		</item>
		<item>
		<title>LXR is a negative regulator of glucose uptake in human adipocytes.</title>
		<link>http://www.brisbanepodiatry.net.au/2013/lxr-is-a-negative-regulator-of-glucose-uptake-in-human-adipocytes-2/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/lxr-is-a-negative-regulator-of-glucose-uptake-in-human-adipocytes-2/#comments</comments>
		<pubDate>Mon, 17 Jun 2013 07:55:08 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Podiatry]]></category>
		<category><![CDATA[adipocytes.]]></category>
		<category><![CDATA[glucose]]></category>
		<category><![CDATA[Human]]></category>
		<category><![CDATA[negative]]></category>
		<category><![CDATA[regulator]]></category>
		<category><![CDATA[uptake]]></category>

		<guid isPermaLink="false">http://www.brisbanepodiatry.net.au/2013/lxr-is-a-negative-regulator-of-glucose-uptake-in-human-adipocytes-2/</guid>
		<description><![CDATA[Related Articles LXR is a negative regulator of glucose uptake in human adipocytes. Diabetologia. 2013 Jun 15; Authors: Pettersson AM, Stenson BM, Lorente-Cebrián S, Andersson DP, Mejhert N, Krätzel J, Aström G, Dahlman I, Chibalin AV, Arner P, Laurencikiene J Abstract AIMS/HYPOTHESIS: Obesity increases the risk of developing type 2 diabetes mellitus, characterised by impaired [...]]]></description>
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<tr>
<td align="left"/>
<td align="right">Related Articles</td>
</tr>
</table>
<p><b>LXR is a negative regulator of glucose uptake in human adipocytes.</b></p>
<p>Diabetologia. 2013 Jun 15;</p>
<p>Authors:  Pettersson AM, Stenson BM, Lorente-Cebrián S, Andersson DP, Mejhert N, Krätzel J, Aström G, Dahlman I, Chibalin AV, Arner P, Laurencikiene J</p>
<p>Abstract<br/><br />
        AIMS/HYPOTHESIS: Obesity increases the risk of developing type 2 diabetes mellitus, characterised by impaired insulin-mediated glucose uptake in peripheral tissues. Liver X receptor (LXR) is a positive regulator of adipocyte glucose transport in murine models and a possible target for diabetes treatment. However, the levels of LXRα are increased in obese adipose tissue in humans. We aimed to investigate the transcriptome of LXR and the role of LXR in the regulation of glucose uptake in primary human adipocytes. METHODS: The insulin responsiveness of human adipocytes differentiated in vitro was characterised, adipocytes were treated with the LXR agonist GW3965 and global transcriptome profiling was determined by microarray, followed by quantitative RT-PCR (qRT-PCR), western blot and ELISA. Basal and insulin-stimulated glucose uptake was measured and the effect on plasma membrane translocation of glucose transporter 4 (GLUT4) was assayed. RESULTS: LXR activation resulted in transcriptional suppression of several insulin signalling genes, such as AKT2, SORBS1 and CAV1, but caused only minor changes (&lt;15%) in microRNA expression. Activation of LXR impaired the plasma membrane translocation of GLUT4, but not the expression of its gene, SLC2A4. LXR activation also diminished insulin-stimulated glucose transport and lipogenesis in adipocytes obtained from overweight individuals. Furthermore, AKT2 expression was reduced in obese adipose tissue, and AKT2 and SORBS1 expression was inversely correlated with BMI and HOMA index. CONCLUSIONS/INTERPRETATION: In contrast to murine models, LXR downregulates insulin-stimulated glucose uptake in human adipocytes from overweight individuals. This could be due to suppression of Akt2, c-Cbl-associated protein and caveolin-1. These findings challenge the idea of LXR as a drug target in the treatment of diabetes.<br/>
        </p>
<p>PMID: 23765184 [PubMed - as supplied by publisher]</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/pubmed/23765184?dopt=Abstract">pubmed: diabetologia[journal&#8230;</a></p>
]]></content:encoded>
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		</item>
		<item>
		<title>LXR is a negative regulator of glucose uptake in human adipocytes.</title>
		<link>http://www.brisbanepodiatry.net.au/2013/lxr-is-a-negative-regulator-of-glucose-uptake-in-human-adipocytes/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/lxr-is-a-negative-regulator-of-glucose-uptake-in-human-adipocytes/#comments</comments>
		<pubDate>Mon, 17 Jun 2013 07:55:07 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Podiatry]]></category>
		<category><![CDATA[adipocytes.]]></category>
		<category><![CDATA[glucose]]></category>
		<category><![CDATA[Human]]></category>
		<category><![CDATA[negative]]></category>
		<category><![CDATA[regulator]]></category>
		<category><![CDATA[uptake]]></category>

		<guid isPermaLink="false">http://www.brisbanepodiatry.net.au/2013/lxr-is-a-negative-regulator-of-glucose-uptake-in-human-adipocytes/</guid>
		<description><![CDATA[Related Articles LXR is a negative regulator of glucose uptake in human adipocytes. Diabetologia. 2013 Jun 15; Authors: Pettersson AM, Stenson BM, Lorente-Cebrián S, Andersson DP, Mejhert N, Krätzel J, Aström G, Dahlman I, Chibalin AV, Arner P, Laurencikiene J Abstract AIMS/HYPOTHESIS: Obesity increases the risk of developing type 2 diabetes mellitus, characterised by impaired [...]]]></description>
			<content:encoded><![CDATA[<table border="0" width="100%">
<tr>
<td align="left"/>
<td align="right">Related Articles</td>
</tr>
</table>
<p><b>LXR is a negative regulator of glucose uptake in human adipocytes.</b></p>
<p>Diabetologia. 2013 Jun 15;</p>
<p>Authors:  Pettersson AM, Stenson BM, Lorente-Cebrián S, Andersson DP, Mejhert N, Krätzel J, Aström G, Dahlman I, Chibalin AV, Arner P, Laurencikiene J</p>
<p>Abstract<br/><br />
        AIMS/HYPOTHESIS: Obesity increases the risk of developing type 2 diabetes mellitus, characterised by impaired insulin-mediated glucose uptake in peripheral tissues. Liver X receptor (LXR) is a positive regulator of adipocyte glucose transport in murine models and a possible target for diabetes treatment. However, the levels of LXRα are increased in obese adipose tissue in humans. We aimed to investigate the transcriptome of LXR and the role of LXR in the regulation of glucose uptake in primary human adipocytes. METHODS: The insulin responsiveness of human adipocytes differentiated in vitro was characterised, adipocytes were treated with the LXR agonist GW3965 and global transcriptome profiling was determined by microarray, followed by quantitative RT-PCR (qRT-PCR), western blot and ELISA. Basal and insulin-stimulated glucose uptake was measured and the effect on plasma membrane translocation of glucose transporter 4 (GLUT4) was assayed. RESULTS: LXR activation resulted in transcriptional suppression of several insulin signalling genes, such as AKT2, SORBS1 and CAV1, but caused only minor changes (&lt;15%) in microRNA expression. Activation of LXR impaired the plasma membrane translocation of GLUT4, but not the expression of its gene, SLC2A4. LXR activation also diminished insulin-stimulated glucose transport and lipogenesis in adipocytes obtained from overweight individuals. Furthermore, AKT2 expression was reduced in obese adipose tissue, and AKT2 and SORBS1 expression was inversely correlated with BMI and HOMA index. CONCLUSIONS/INTERPRETATION: In contrast to murine models, LXR downregulates insulin-stimulated glucose uptake in human adipocytes from overweight individuals. This could be due to suppression of Akt2, c-Cbl-associated protein and caveolin-1. These findings challenge the idea of LXR as a drug target in the treatment of diabetes.<br/>
        </p>
<p>PMID: 23765184 [PubMed - as supplied by publisher]</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/pubmed/23765184?dopt=Abstract">pubmed: diabetologia[journal&#8230;</a></p>
]]></content:encoded>
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		</item>
		<item>
		<title>Location-dependent depth and undermining formation of pressure ulcers.</title>
		<link>http://www.brisbanepodiatry.net.au/2013/location-dependent-depth-and-undermining-formation-of-pressure-ulcers/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/location-dependent-depth-and-undermining-formation-of-pressure-ulcers/#comments</comments>
		<pubDate>Mon, 17 Jun 2013 01:54:46 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Podiatry]]></category>
		<category><![CDATA[Depth]]></category>
		<category><![CDATA[Formation]]></category>
		<category><![CDATA[Locationdependent]]></category>
		<category><![CDATA[pressure]]></category>
		<category><![CDATA[Ulcers]]></category>
		<category><![CDATA[undermining]]></category>

		<guid isPermaLink="false">http://www.brisbanepodiatry.net.au/2013/location-dependent-depth-and-undermining-formation-of-pressure-ulcers/</guid>
		<description><![CDATA[Related Articles Location-dependent depth and undermining formation of pressure ulcers. J Tissue Viability. 2013 Jun 11; Authors: Takahashi Y, Isogai Z, Mizokami F, Furuta K, Nemoto T, Kanoh H, Yoneda M Abstract AIM OF THE STUDY: We examined the location-specific properties of pressure ulcers, focusing on depth and undermining formation, which are often unfavorable factors [...]]]></description>
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</table>
<p><b>Location-dependent depth and undermining formation of pressure ulcers.</b></p>
<p>J Tissue Viability. 2013 Jun 11;</p>
<p>Authors:  Takahashi Y, Isogai Z, Mizokami F, Furuta K, Nemoto T, Kanoh H, Yoneda M</p>
<p>Abstract<br/><br />
        AIM OF THE STUDY: We examined the location-specific properties of pressure ulcers, focusing on depth and undermining formation, which are often unfavorable factors for ulcer healing. METHODS: We conducted a retrospective observational study of 2 independent databases on pressure ulcers. Databases from a 200-bed hospital (database A) and a 300-bed hospital (database B) were collected during different time periods. Relationships between ulcer location, ulcer depth, and undermining formation were analyzed. All pressure ulcers were accurately diagnosed and classified according to their locations. RESULTS: A total of 282 pressure ulcers in 189 patients from database A and 232 pressure ulcers in 154 patients from database B were analyzed. It was found that pressure ulcers primarily developed over the sacrum. Ratio of stages III and IV pressure ulcers was high in pressure ulcers of the foot, ankle, and crus on the lower leg. Among the deep pressure ulcers, undermining formation was frequently observed on the greater trochanter, ilium, and sacrum. In contrast, pressure ulcers of the foot, ankle, and crus did not exhibit undermining formation. CONCLUSION: Our results revealed marked differences in pressure ulcer properties depending on their location. Factors affecting depth and undermining of pressure ulcers appear to be related to anatomical and physical properties of the bone and subcutaneous tissue.<br/>
        </p>
<p>PMID: 23764355 [PubMed - as supplied by publisher]</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/pubmed/23764355?dopt=Abstract">pubmed: ankle</a></p>
]]></content:encoded>
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		</item>
		<item>
		<title>Pulsed radio frequency energy therapy use for pain relief following surgery for tendinopathy-associated chronic pain: two case reports.</title>
		<link>http://www.brisbanepodiatry.net.au/2013/pulsed-radio-frequency-energy-therapy-use-for-pain-relief-following-surgery-for-tendinopathy-associated-chronic-pain-two-case-reports/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/pulsed-radio-frequency-energy-therapy-use-for-pain-relief-following-surgery-for-tendinopathy-associated-chronic-pain-two-case-reports/#comments</comments>
		<pubDate>Sun, 16 Jun 2013 22:54:43 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Podiatry]]></category>
		<category><![CDATA[Case]]></category>
		<category><![CDATA[chronic]]></category>
		<category><![CDATA[Energy]]></category>
		<category><![CDATA[following]]></category>
		<category><![CDATA[Frequency]]></category>
		<category><![CDATA[Pain]]></category>
		<category><![CDATA[pulsed]]></category>
		<category><![CDATA[Radio]]></category>
		<category><![CDATA[Relief]]></category>
		<category><![CDATA[Reports]]></category>
		<category><![CDATA[Surgery]]></category>
		<category><![CDATA[tendinopathyassociated]]></category>
		<category><![CDATA[Therapy]]></category>

		<guid isPermaLink="false">http://www.brisbanepodiatry.net.au/2013/pulsed-radio-frequency-energy-therapy-use-for-pain-relief-following-surgery-for-tendinopathy-associated-chronic-pain-two-case-reports/</guid>
		<description><![CDATA[Related Articles Pulsed radio frequency energy therapy use for pain relief following surgery for tendinopathy-associated chronic pain: two case reports. Mil Med. 2013 Jan;178(1):e125-9 Authors: Cortes J, Kubat N, Japour C Abstract Chronic tendon pain from overuse is a common condition, with limited options for ongoing pain management. Two cases are presented in which pulsed [...]]]></description>
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</table>
<p><b>Pulsed radio frequency energy therapy use for pain relief following surgery for tendinopathy-associated chronic pain: two case reports.</b></p>
<p>Mil Med. 2013 Jan;178(1):e125-9</p>
<p>Authors:  Cortes J, Kubat N, Japour C</p>
<p>Abstract<br/><br />
        Chronic tendon pain from overuse is a common condition, with limited options for ongoing pain management. Two cases are presented in which pulsed radio frequency energy (PRFE) therapy was used for pain relief following surgical intervention for chronic tendinopathy-associated pain, unresponsive to conventional therapies. Both patients showed a dramatic reduction in pain following PRFE therapy after 2 to 3 weeks of treatment, and at the 7-month (case 1) and 6-month (case 2) follow-up visits, both patients reported that pain had not returned. Recent molecular evidence suggests a possible mechanism underlying PRFE-mediated pain relief. Further study into this promising technology is warranted.<br/>
        </p>
<p>PMID: 23764157 [PubMed - in process]</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/pubmed/23764157?dopt=Abstract">pubmed: podiatry</a></p>
]]></content:encoded>
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		</item>
		<item>
		<title>The relationship between dipper/nondipper pattern and cardioankle vascular index in hypertensive diabetic patients.</title>
		<link>http://www.brisbanepodiatry.net.au/2013/the-relationship-between-dippernondipper-pattern-and-cardioankle-vascular-index-in-hypertensive-diabetic-patients/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/the-relationship-between-dippernondipper-pattern-and-cardioankle-vascular-index-in-hypertensive-diabetic-patients/#comments</comments>
		<pubDate>Sun, 16 Jun 2013 19:55:41 +0000</pubDate>
		<dc:creator>admin</dc:creator>
				<category><![CDATA[Podiatry]]></category>
		<category><![CDATA[between]]></category>
		<category><![CDATA[cardioankle]]></category>
		<category><![CDATA[Diabetic]]></category>
		<category><![CDATA[dipper/nondipper]]></category>
		<category><![CDATA[hypertensive]]></category>
		<category><![CDATA[index]]></category>
		<category><![CDATA[Patients]]></category>
		<category><![CDATA[Pattern]]></category>
		<category><![CDATA[Relationship]]></category>
		<category><![CDATA[vascular]]></category>

		<guid isPermaLink="false">http://www.brisbanepodiatry.net.au/2013/the-relationship-between-dippernondipper-pattern-and-cardioankle-vascular-index-in-hypertensive-diabetic-patients/</guid>
		<description><![CDATA[Related Articles The relationship between dipper/nondipper pattern and cardioankle vascular index in hypertensive diabetic patients. Blood Press Monit. 2013 Jun 12; Authors: Kalaycioğlu E, Gökdeniz T, Aykan AC, Gül I, Dursun I, Kiriş G, Celik S Abstract OBJECTIVE: 24-h ambulatory blood pressure monitoring (24-h ABPM) is a better predictor of cardiovascular events (CVEs) than spot [...]]]></description>
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<p><b>The relationship between dipper/nondipper pattern and cardioankle vascular index in hypertensive diabetic patients.</b></p>
<p>Blood Press Monit. 2013 Jun 12;</p>
<p>Authors:  Kalaycioğlu E, Gökdeniz T, Aykan AC, Gül I, Dursun I, Kiriş G, Celik S</p>
<p>Abstract<br/><br />
        OBJECTIVE: 24-h ambulatory blood pressure monitoring (24-h ABPM) is a better predictor of cardiovascular events (CVEs) than spot blood pressure (BP) measurements in hypertensive diabetic patients. In this patient group, the underlying mechanism of the relationship between a nondipper pattern determined with 24-h ABPM and increased incidence of CVE is unknown. Cardioankle vascular index (CAVI) is a new index of the overall arterial stiffness from the aorta to the ankle. The objective of the present study was to evaluate the relationship between a dipper/nondipper pattern and arterial stiffness in hypertensive diabetic patients using the CAVI method. METHODS: We enrolled 99 hypertensive patients with type-2 diabetes mellitus. 24-h ABPM and CAVI measurements were performed for all patients. The relationship between a dipper/nondipper pattern and CAVI measurements was analyzed. RESULTS: Sixty-three (63.6%) patients had a nondipper pattern. In univariate analysis, CAVI, mean arterial pressure (MAP)-asleep, overall diastolic BP, overall systolic BP, duration of hypertension, and statin use were significantly higher among patients with a nondipper pattern than that in dippers. Multivariate linear regression analyses showed that the difference between MAP-asleep and MAP-awake was associated independently with CAVI (β coefficient=0.514, P&lt;0.001). CAVI was correlated negatively with the nocturnal decrease in MAP (%) (r=-0.558 and P&lt;0.001). CONCLUSION: The nondipper pattern determined with 24-h ABPM in hypertensive diabetic patients is associated with an increase in arterial stiffness. This patient group should be monitored closely for CVEs.<br/>
        </p>
<p>PMID: 23764917 [PubMed - as supplied by publisher]</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/pubmed/23764917?dopt=Abstract">pubmed: ankle</a></p>
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		<title>Roux-en-Y gastric bypass vs sleeve gastrectomy for obese patients with type 2 diabetes: a randomised trial.</title>
		<link>http://www.brisbanepodiatry.net.au/2013/roux-en-y-gastric-bypass-vs-sleeve-gastrectomy-for-obese-patients-with-type-2-diabetes-a-randomised-trial/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/roux-en-y-gastric-bypass-vs-sleeve-gastrectomy-for-obese-patients-with-type-2-diabetes-a-randomised-trial/#comments</comments>
		<pubDate>Sun, 16 Jun 2013 13:54:40 +0000</pubDate>
		<dc:creator>admin</dc:creator>
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		<guid isPermaLink="false">http://www.brisbanepodiatry.net.au/2013/roux-en-y-gastric-bypass-vs-sleeve-gastrectomy-for-obese-patients-with-type-2-diabetes-a-randomised-trial/</guid>
		<description><![CDATA[Related Articles Roux-en-Y gastric bypass vs sleeve gastrectomy for obese patients with type 2 diabetes: a randomised trial. Diabetologia. 2013 Jun 14; Authors: Keidar A, Hershkop KJ, Marko L, Schweiger C, Hecht L, Bartov N, Kedar A, Weiss R Abstract AIMS/HYPOTHESIS: Bariatric surgery is gaining acceptance as a &#8216;metabolic surgical intervention&#8217; for patients with type [...]]]></description>
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<p><b>Roux-en-Y gastric bypass vs sleeve gastrectomy for obese patients with type 2 diabetes: a randomised trial.</b></p>
<p>Diabetologia. 2013 Jun 14;</p>
<p>Authors:  Keidar A, Hershkop KJ, Marko L, Schweiger C, Hecht L, Bartov N, Kedar A, Weiss R</p>
<p>Abstract<br/><br />
        AIMS/HYPOTHESIS: Bariatric surgery is gaining acceptance as a &#8216;metabolic surgical intervention&#8217; for patients with type 2 diabetes. The optimal form of surgery and the mechanism of action of these procedures are much debated. We compared two bariatric procedures for obese patients with type 2 diabetes and evaluated their effects on HbA1c and glucose tolerance. METHODS: We performed a parallel un-blinded randomised trial of Roux-en-Y gastric bypass (RYGB) vs sleeve gastrectomy (SG) in 41 obese patients with type 2 diabetes, who were bariatric surgery candidates attending the obesity clinic. HbA1c, body composition and glucose tolerance were evaluated at baseline, and at 3 and 12 months. RESULTS: Of the 41 patients, 37 completed the follow-up (19 RYGB, 18 SG). Both groups had similar baseline anthropometric and biochemical measures, and showed comparable weight loss and fat:fat-free mass ratio changes at 12 months. A similar normalisation of HbA1c levels was observed as early as 3 months post-surgery (6.37 ± 0.71% vs 6.23 ± 0.69% for RYGB vs SG respectively, p &lt; 0.001 in both groups for baseline vs follow-up). CONCLUSIONS/INTERPRETATION: In this study, RYGB did not have a superior effect in comparison to SG with regard to HbA1c levels or weight loss during 12 months of follow-up. TRIAL REGISTRATION: ClinicalTrials.gov NCT00667706 FUNDING: This work was supported by grant no. 3-000-8480 from the Israel Ministry of Health Chief Scientist, the Stephen Morse Diabetes Research Foundation and by Johnson &amp; Johnson.<br/>
        </p>
<p>PMID: 23765186 [PubMed - as supplied by publisher]</p>
<p><a rel="nofollow" href="http://www.ncbi.nlm.nih.gov/pubmed/23765186?dopt=Abstract">pubmed: diabetologia[journal&#8230;</a></p>
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		<title>foot; +17 new citations</title>
		<link>http://www.brisbanepodiatry.net.au/2013/foot-17-new-citations-14/</link>
		<comments>http://www.brisbanepodiatry.net.au/2013/foot-17-new-citations-14/#comments</comments>
		<pubDate>Sun, 16 Jun 2013 10:54:37 +0000</pubDate>
		<dc:creator>admin</dc:creator>
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		<guid isPermaLink="false">http://www.brisbanepodiatry.net.au/2013/foot-17-new-citations-14/</guid>
		<description><![CDATA[17 new pubmed citations were retrieved for your search. Click on the search hyperlink below to display the complete search results: foot These pubmed results were generated on 2013/06/16 PubMed, a service of the National Library of Medicine, includes over 15 million citations for biomedical articles back to the 1950&#8242;s. These citations are from MEDLINE [...]]]></description>
			<content:encoded><![CDATA[<p>17 new pubmed citations were retrieved for your search.<br />
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<p align="center"><b>foot</b></p>
<p>These pubmed results were generated on 2013/06/16</p>
<p>PubMed, a service of the National Library of Medicine, includes over 15 million<br />
citations for biomedical articles back to the 1950&#8242;s.<br />
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