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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.arcmedres.com/?rss=yes"><title>Archives of Medical Research</title><description>Archives of Medical Research RSS feed: Current Issue. 
 
 Archives of Medical Research  publishes original peer-reviewed medical research in an attempt to bridge 
the gaps created by medical specialization. Contributions are grouped into three main categories - biomedical, clinical, and epidemiological. 
Review articles, outstanding case reports, and preliminary communications will also be considered. As an international publication, the 
study of diseases is presented from various perspectives to provide the medical community with original investigation from molecular 
biology to clinical epidemiology within a single publication.</description><link>http://www.arcmedres.com/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2009 Published by Elsevier Inc. All rights reserved. </dc:rights><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:issn>0188-4409</prism:issn><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:publicationDate>October 2009</prism:publicationDate><prism:copyright> © 2009 Published by Elsevier Inc. All rights reserved. </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909002045/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001957/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001611/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001829/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001854/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001301/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001313/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001374/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001350/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001416/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001386/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001362/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001490/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001507/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001519/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001520/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS018844090900188X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001817/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001489/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909001866/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909002185/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909002057/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909002069/abstract?rss=yes"/><rdf:li rdf:resource="http://www.arcmedres.com/article/PIIS0188440909002173/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909002045/abstract?rss=yes"><title>Copyright</title><link>http://www.arcmedres.com/article/PIIS0188440909002045/abstract?rss=yes</link><description></description><dc:title>Copyright</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0188-4409(09)00204-5</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IFC</prism:startingPage><prism:endingPage>IFC</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001957/abstract?rss=yes"><title>Fifty years after C.P. Snow. The “Two Medical Cultures”</title><link>http://www.arcmedres.com/article/PIIS0188440909001957/abstract?rss=yes</link><description>Fifty years ago Charles Percy Snow delivered a highly influential lecture that he named “The Two Cultures” at Cambridge University. He contrasted science, the one culture vs. humanities, the second culture in the context of academic and social views. The center of his hypothesis was that there was a big gulf between the cultures, science and humanities, and that there was scarce, if not a lack of, communication between these disciplines. He lamented that the division between science and humanities could impede social progress. Snow was concerned that a world without science may lead to an unhealthy society. He thus advocated a cross-talk between disciplines as a necessary way to bridge the gap of misunderstanding between the cultures. He contended that it would be necessary to find ways to translate highly complex scientific information to a nonscientific process of political decision making in different areas of social concern such as military or medical. He explained that the main reason for this regrettable division was that, in almost all countries, the gap was already widened by the time students enter university. Students had already been driven to one of two different paths: science or humanities.</description><dc:title>Fifty years after C.P. Snow. The “Two Medical Cultures”</dc:title><dc:creator>Luis Benítez-Bribiesca</dc:creator><dc:identifier>10.1016/j.arcmed.2009.10.006</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Editorial</prism:section><prism:startingPage>525</prism:startingPage><prism:endingPage>526</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001611/abstract?rss=yes"><title>Repeated Dose Toxicity Study of a Live Attenuated Oral Cholera Vaccine in Sprague Dawley Rats</title><link>http://www.arcmedres.com/article/PIIS0188440909001611/abstract?rss=yes</link><description>Background and Aims: A live attenuated vaccine candidate against human cholera has been developed from the genetically modified Vibrio cholerae O1, biotype El Tor, serotype Ogawa, 638 strain. Previous single dose toxicity and local tolerance studies have demonstrated that the product is innocuous in Sprague Dawley rats by oral route and single dose. The present paper describes a repeated dose toxicity study using a further dose compared to the proposed clinical schedule.Methods: Sprague Dawley rats (140–180g) were treated with two doses of the vaccine candidate with a dedicated placebo formulation or were not treated at all (controls). The test products were inoculated at a 21-day interval. Animals were observed daily, body weight was determined weekly and food and water intakes were measured every other day. Three and 14 days after the last inoculation, groups of rats were humanely sacrificed, bled and macroscopically examined. Blood samples were taken for hematology, serum biochemistry and to determine the vibriocide antibody titers. A comprehensive list of tissue and organ samples was taken for microscopic studies.Results: There was no mortality and no animal showed any clinical symptoms. Food and water intake, body weight, and hematological and biochemical variables did not show differences of toxicological and/or statistical relevance among the experimental groups. Macroscopic examination did not demonstrate any alterations and there were no histological findings of toxicological significance.Conclusions: The vaccine was considered potentially safe for human use as indicated by the results in Sprague Dawley rats.</description><dc:title>Repeated Dose Toxicity Study of a Live Attenuated Oral Cholera Vaccine in Sprague Dawley Rats</dc:title><dc:creator>Sergio Sifontes-Rodríguez, Juan Francisco Infante-Bourzac, Daiyana Díaz-Rivero, Yulieé López-Feria, Merlin Pérez-Pérez, Eligio Sosa-Roble, Viviana Pérez-Amat, Yamilé López-Hernández, Eduardo Álvarez-Figueredo, Juan Carlos Martínez-Rodríguez, Mildrey Fariñas-Medina, Tamara Hernández-Salazar, Yolexis Tamayo-García, Yolanda Valdés-Abreu, Adriana Ponce-Collera, Niurka Rodríguez-Pérez</dc:creator><dc:identifier>10.1016/j.arcmed.2009.09.003</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>527</prism:startingPage><prism:endingPage>535</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001829/abstract?rss=yes"><title>Effect of Dipeptidyl Peptidase-IV (DPP-IV) Inhibitor (Vildagliptin) on Peripheral Nerves in Streptozotocin-induced Diabetic Rats</title><link>http://www.arcmedres.com/article/PIIS0188440909001829/abstract?rss=yes</link><description>Background and Aims: The aim of this study was to investigate the GLP-1 pathway effect on peripheral nerves using a DPP-IV inhibitor in streptozotocin (STZ)-induced diabetic rats.Methods: Adult male Sprague Dawley rats were divided into four groups and two groups (n=6 in each) were given a DPP-IV inhibitor of 0.3mg/kg/day or 10mg/kg/day dissolved in water. Intraepidermal innervation was quantified as nerve fiber abundance per unit length of epidermis (IENF/mm) following an immunohistochemical procedure using the polyclonal antibody of anti-protein gene product 9.5 (PGP 9.5).Results: Daily administration of DPP-IV inhibitor to the experimental diabetes model at doses of 10mg/kg for 32 weeks protected nerve fiber loss compared with untreated rats as follows (IENF/mm): normal (9.89±0.34), diabetes mellitus (DM) (8.42±0.28), DM with 0.3mg/kg DPP-IV inhibitor (9.88±0.38), and DM with 10mg/kg DPP-IV inhibitor (10.36±0.32) (p&lt;0.05). There was a significant reduction (% change) in the decrease of intraepidermal nerve fiber density (IENFD) in the DPP-IV inhibitor-treated groups during the experimental period: normal (10.1%), DM (25.8%), DM with 0.3mg/kg DPP-IV inhibitor (13.3%), and DM with 10mg/kg DPP-IV inhibitor (7.9%) (p&lt;0.05).Conclusions: Our study suggests that a DPP-IV inhibitor may prevent peripheral nerve degeneration in a diabetes-induced animal model and support the idea that GLP-1 may be useful in peripheral neuropathy.</description><dc:title>Effect of Dipeptidyl Peptidase-IV (DPP-IV) Inhibitor (Vildagliptin) on Peripheral Nerves in Streptozotocin-induced Diabetic Rats</dc:title><dc:creator>Heung Yong Jin, Wei Jing Liu, Ji Hyun Park, Hong Sun Baek, Tae Sun Park</dc:creator><dc:identifier>10.1016/j.arcmed.2009.09.005</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>536</prism:startingPage><prism:endingPage>544</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001854/abstract?rss=yes"><title>Neurite Outgrowth on Chromaffin Cells Applying Extremely Low Frequency Magnetic Fields by Permanent Magnets</title><link>http://www.arcmedres.com/article/PIIS0188440909001854/abstract?rss=yes</link><description>Background and Aims: There is an increasing interest about the effects of electromagnetic fields on health and clinical applications. Electromagnetic fields have been shown to promote differentiation and regeneration of many tissues. The purpose of the present study was to evaluate if a magnetic field (MF) varying in time is able to induce neurite outgrowth in cultured chromaffin cells. For this reason, a stimulation system was developed in order to generate a magnetic field, using permanent magnets as a supply.Methods: In this investigation we used a pair of permanent ferrite magnets. These were mounted in a mechanical system in which both magnets rotate around a culture Petri dish. The stimulation device was designed at Centro de Investigación y de Estudios Avanzados, Avanzados del IPN, Mexico City. Primary cultures of chromaffin cells were stimulated with a magnetic field of 6.4 mT and 4, 7, 10 or 12Hz (2h daily, during a 7-day period). After treatment, percentage of neurite outgrowth was calculated.Results: Our results show that the magnetic fields produced by rotating permanent magnets induced neurite outgrowth on chromaffin cells at 7 and 10Hz.Conclusions: The present study provides evidence that MFs varying in time (7 and 10Hz) induce neurite outgrowth in chromaffin cells. These studies will contribute to elucidate the effect of noninvasive MF stimulus in order to apply it in future regeneration therapies. Also, the device designed could be used for different kind of cells and may work as a model for future clinical devices.</description><dc:title>Neurite Outgrowth on Chromaffin Cells Applying Extremely Low Frequency Magnetic Fields by Permanent Magnets</dc:title><dc:creator>Hugo Hernández-Hernández, Hugo Cruces-Solis, David Elías-Viñas, Leticia Verdugo-Díaz</dc:creator><dc:identifier>10.1016/j.arcmed.2009.10.002</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>545</prism:startingPage><prism:endingPage>550</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001301/abstract?rss=yes"><title>DNA Copy Number Changes in Gastric Adenocarcinomas: High Resolution–Comparative Genomic Hybridization Study in Turkey</title><link>http://www.arcmedres.com/article/PIIS0188440909001301/abstract?rss=yes</link><description>Background and Aims: Multiple genetic alterations are responsible for development and progression of gastric cancer which is one of the leading causes of cancer-related deaths worldwide. The aim of this study was to identify the genomic imbalances of gains and/or losses in gastric adenocarcinomas from Turkish patients and to investigate their association with development and progression of this type of cancer.Methods: Forty three patients with gastric adenocarcinoma were enrolled in this study and genomic imbalances were analyzed by high-resolution–comparative genomic hybridization (HR–CGH).Results: In 36/43 cases (84%) of gastric adenocarcinomas, genomic imbalances have involved all chromosomes in various combinations. The mean number of gains was 3.95±4.19 and the most common gains observed were 7q (35%), 8q (35%), 7p (28%), 1q (26%), 13q (26%), and 20q (21%). The calculated mean number of losses was 3.65±3.55 and the most common losses were found on arms 18q (26%), 5q (21%), and 14q (21%). High-level amplifications involved chromosomes 1, 7, 8, 9, 13, and 16. No significant differences in chromosomal imbalances were observed in different tumor stages, tumor grades, and Helicobacter pylori infection status groups. The most striking result in this study was the involvement of the 13q gains with increased lymph node metastasis (p=0.046). Late-stage tumors displayed a somewhat significantly higher number of losses than early-stage tumors (p=0.053).Conclusions: A series of gains, losses and amplifications concerned with gastric adenocarcinoma identified in this study are presented in detail. In particular, 13q21–q32 was prominent because it has been linked to increased lymph node metastasis.</description><dc:title>DNA Copy Number Changes in Gastric Adenocarcinomas: High Resolution–Comparative Genomic Hybridization Study in Turkey</dc:title><dc:creator>Güvem Gümüs-Akay, Ali Ekrem Ünal, Atilla Halil Elhan, Sancar Bayar, Kürsat Karadayι, Asuman Sunguroglu, Ahmet Kadıkıran, Ajlan Tükün</dc:creator><dc:identifier>10.1016/j.arcmed.2009.07.004</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>551</prism:startingPage><prism:endingPage>560</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001313/abstract?rss=yes"><title>Does Defective Apoptosis Play A Role in Cystic Fibrosis Lung Disease?</title><link>http://www.arcmedres.com/article/PIIS0188440909001313/abstract?rss=yes</link><description>Background and Aims: Although apoptotic dysfunction has recently been suggested in cystic fibrosis (CF), there are few studies reported concerning apoptosis in CF with controversial results. The aim of this study was to investigate apoptosis in CF human lung tissues and compare with non-CF bronchiectatic and normal healthy lung tissues. We also investigated the relation between apoptosis and histopathological features of tissues and microbiological factors influencing apoptosis.Methods: Lung tissue samples from CF (n=30), non-CF bronchiectasis (n=28, BE group) and normal control cases (n=24, C group) were included in the study. Histological examination of H &amp; E-stained archived slides was performed and TUNEL method was used to detect DNA fragmentation.Results: Apoptotic alveolar epithelial cells were significantly increased in the CF group compared to BE and C groups (p=0.046). Bronchopneumonia (BP) was present in 15 CF cases (50%), whereas none of the cases in C group had BP (p=0.0001). Apoptosis was significantly increased in cases with BP (n=17) compared to cases without BP (n=65) (p=0.04).Conclusions: Apoptotic epithelial cells and BP were significantly increased in the CF group and excess level of apoptosis may be the result of enhanced occurrence of BP. Apoptotic cells were alveolar epithelial cells in the great majority of the patients and were not detected in other locations where CFTR expression is much more prominent than alveolar cells. We may postulate that increased apoptotic findings in the alveolar epithelium were related with the presence of chronic infections rather than CFTR dysfunction.</description><dc:title>Does Defective Apoptosis Play A Role in Cystic Fibrosis Lung Disease?</dc:title><dc:creator>Ebru Yalçin, Beril Talim, Uğur Özçelik, Deniz Doğru, Nazan Çobanoğlu, Sevgi Pekcan, Nural Kiper</dc:creator><dc:identifier>10.1016/j.arcmed.2009.07.005</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-09-27</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-09-27</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>561</prism:startingPage><prism:endingPage>564</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001374/abstract?rss=yes"><title>A Single Nucleotide Polymorphism in the Vascular Endothelial Growth Factor Gene Is Associated with Recurrence of Hepatocellular Carcinoma after Transplantation</title><link>http://www.arcmedres.com/article/PIIS0188440909001374/abstract?rss=yes</link><description>Background: Vascular endothelial growth factor (VEGF), an important regulator of angiogenesis and vascular permeability, is involved in various steps of many malignancies. Gene polymorphisms within the gene encoding VEGF have been shown to be independently associated with an adverse outcome in various malignancies including hepatocellular carcinoma (HCC) with resection. However, no data are available for HCC treated with liver transplantation (LT). Therefore, we investigated association of VEGF genomic polymorphisms with risk for developing HCC and tumor recurrence after LT.Methods: Seven polymorphisms in the VEGF gene (rs699947, rs1570360, rs2010963, rs3024997, rs3025010, rs3025035, rs3025039) were examined in 93 HCC patients treated with LT and 99 controls using Applied Biosystems SNaP-Shot and TaqMan technology. Cox proportional hazard model was used to estimate the hazard ratios associated with polymorphisms.Results: The association between rs3025035 and recurrence was significant (p=0.003). However, no other SNP in VEGF was associated with recurrence. Interestingly, we found that patients with rs3025035 CT heterozygous was independently associated with a shortened recurrence-free survival (odds ratio: 3.3; 95% confidence interval: 1.8–6.0; p&lt;0.001).Conclusions: Our data suggest that polymorphism rs3025035 in the VEGF gene may be a potential genetic marker for HCC recurrence in LT patients.</description><dc:title>A Single Nucleotide Polymorphism in the Vascular Endothelial Growth Factor Gene Is Associated with Recurrence of Hepatocellular Carcinoma after Transplantation</dc:title><dc:creator>Li-Ming Wu, Hai-Yang Xie, Lin Zhou, Zhe Yang, Feng Zhang, Shu-Sen Zheng</dc:creator><dc:identifier>10.1016/j.arcmed.2009.07.011</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-09-27</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-09-27</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>565</prism:startingPage><prism:endingPage>570</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001350/abstract?rss=yes"><title>High Prevalence of Coronary Heart Disease in Type 2 Diabetic Patients with Non-alcoholic Fatty Liver Disease</title><link>http://www.arcmedres.com/article/PIIS0188440909001350/abstract?rss=yes</link><description>Background and Aims: Nonalcoholic fatty liver disease (NAFLD) is closely associated with insulin resistance and metabolic syndrome. Prevalence of NAFLD increases greatly in patients with type 2 diabetes mellitus (T2DM), and it may also increase cardiovascular disease mortality and morbidity. The aim of our study was to investigate the prevalence of NAFLD in T2DM population and to compare the prevalence of coronary heart disease (CHD) and its risk factors between diabetic patients with and without NAFLD in a Chinese population.Methods: A cross-sectional survey was conducted among 560 cases of in-patient T2DM patients from January 2002 to January 2009 in southern China. Patients were divided into two groups (NAFLD and non-NAFLD) and underwent clinical examination, anthropometry, laboratory tests and routine liver ultrasonography.Results: Prevalence of NAFLD was 75.18% (421 cases) among all participants, and 285 cases (67.70%) had normal liver function and no symptoms. NAFLD group had higher body mass index (BMI), waist/hip circumference ratio (WHR), alanine aminotransferase (ALT), triglycerides (TG) and low-density lipoprotein cholesterol (LDL-C) levels than those without NAFLD (p&lt;0.01). Moreover, the prevalence of CHD was also higher in the NAFLD group (p&lt;0.01), especially in those male patients with elevated plasma ALT.Conclusions: NAFLD is a common condition among T2DM patients. Its occurrence may be related to sex, age, abdominal obesity, dyslipidemia metabolism, etc. and it is associated with a higher prevalence of CHD. Plasma ALT levels may act as a marker.</description><dc:title>High Prevalence of Coronary Heart Disease in Type 2 Diabetic Patients with Non-alcoholic Fatty Liver Disease</dc:title><dc:creator>Hongyun Lu, Longyi Zeng, Biao Liang, Xiaochun Shu, Danhong Xie</dc:creator><dc:identifier>10.1016/j.arcmed.2009.07.009</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-09-27</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-09-27</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>571</prism:startingPage><prism:endingPage>575</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001416/abstract?rss=yes"><title>Effect of Body Weight and Esophageal Damage on the Severity of Gastroesophageal Reflux Symptoms. Mexican GERD Working Group</title><link>http://www.arcmedres.com/article/PIIS0188440909001416/abstract?rss=yes</link><description>Background and Aims: Several studies have demonstrated overweight and obesity are strong independent risk factors of GERD symptoms and esophageal erosions. Our aim was to analyze the joint effect of BMI with the grade of esophageal damage over symptoms' intensity of GERD.Methods: We used a questionnaire with a Likert scale for severity of symptoms related to GERD. The distal portion of the esophagus was evaluated to determine the presence of mucosal injury, classified by Los Angeles criteria (LA).Results: We included 917 subjects (53.76% females) with average age 36.8±7 years. Males had higher BMI than females (26.8±3.5 vs. 25.2±4.5, p&lt;0.001). Severe damage (C–D ulcers) was associated with overweight (BMI 25–30), severity of heartburn,retching, halitosis, regurgitation, and chest oppression. BMI &gt;30 had high score for heartburn and retching, but low score for nausea, compared with lower weight. The model with interaction showed a non-linear association between BMI and LA. Overweight (but not obese) patients with damage scored C–D had the highest score for intensity of heartburn and retching.Conclusions: BMI and LA do not have additive effects on the severity of symptoms of GERD. Those with BMI between 25 and 30 had severe symptoms score, but those with BMI &gt;30 showed lower scores. These findings could explain controversial results found in other studies.</description><dc:title>Effect of Body Weight and Esophageal Damage on the Severity of Gastroesophageal Reflux Symptoms. Mexican GERD Working Group</dc:title><dc:creator>Juan Carlos Lopez-Alvarenga, José Antonio Vargas, Luis Humberto Lopez, Ronnie Fass, Sergio Sobrino-Cossio, Paul Higgins, Anthony Comuzzie</dc:creator><dc:identifier>10.1016/j.arcmed.2009.08.003</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>576</prism:startingPage><prism:endingPage>581</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001386/abstract?rss=yes"><title>Association Between Serum γ-Glutamyltransferase and Acute Ischemic Nonembolic Stroke in Elderly Subjects</title><link>http://www.arcmedres.com/article/PIIS0188440909001386/abstract?rss=yes</link><description>Abstract: Background and Aims: Elevated serum γ-glutamyltransferase (GGT) levels have been proposed as an independent predictor for cardiovascular morbidity and mortality. The aim of this study was to determine whether GGT levels are associated with acute ischemic/nonembolic stroke in a case-control study of elderly subjects.Methods: A total of 163 patients &gt;70 years of age (88 men) admitted due to a first-ever acute ischemic/nonembolic stroke and 166 volunteers (87 men) without a history of cardiovascular disease were included. The association between GGT and stroke was determined by multivariate logistic regression modelling after adjusting for potential confounding factors.Results: GGT levels were higher in subjects with metabolic syndrome (MetS) and correlated with MetS individual components including insulin resistance. Stroke patients showed higher concentrations of GGT compared with controls. In univariate analysis, crude odds ratio (OR) for GGT was 1.06/1 IU/L increase (95% CI, 1.03−1.09; p&lt;0.001). Compared to subjects with GGT levels in the lowest quartile, those within the highest quartile had a 4.7-times increase in the odds of experiencing an ischemic stroke (95% CI 2.39-9.11, p&lt;0.001). This association remained significant after controlling for all potential confounders (adjusted OR, 2.90, 95% CI, 1.35−6.27; p=0.007). Analysis of interaction between MetS and GGT showed that subjects with MetS had a 1.08 higher odds/1 IU/L increase in GGT to experience an ischemic stroke [adjusted OR, 1.08 (95% CI, 1.04−1.12; p&lt;0.001).Conclusions: There are positive associations between serum GGT and first ischemic/nonembolic stroke in individuals &gt;70 years of age independent of established risk factors for cardiovascular disease and concurrent metabolic abnormalities.</description><dc:title>Association Between Serum γ-Glutamyltransferase and Acute Ischemic Nonembolic Stroke in Elderly Subjects</dc:title><dc:creator>Panagiotis Korantzopoulos, Petros Tzimas, Kallirroi Kalantzi, Michael Kostapanos, Konstantinos Vemmos, John Goudevenos, Moses Elisaf, Haralampos Milionis</dc:creator><dc:identifier>10.1016/j.arcmed.2009.07.012</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>582</prism:startingPage><prism:endingPage>589</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001362/abstract?rss=yes"><title>Elevated Circulating and Synovial Fluid Endoglin Are Associated with Primary Knee Osteoarthritis Severity</title><link>http://www.arcmedres.com/article/PIIS0188440909001362/abstract?rss=yes</link><description>Background and Aims: Osteoarthritis (OA) is a chronic degenerative joint disorder of the synovial joint characterized by loss of articular cartilage, osteophyte formation, and alterations of subchondral bone. The aim of this study was to evaluate endoglin levels in both plasma and synovial fluid of patients with primary knee OA and to determine their relationship with disease severity.Methods: Thirty nine patients with primary knee OA and 15 healthy controls were recruited in this study. The radiographic grading of OA in the knee was performed using the Kellgren and Lawrence classification. Endoglin concentrations in both plasma and synovial fluid were analyzed using a sandwich enzyme-linked immunosorbent assay.Results: The average value of plasma endoglin in patients with knee OA was significantly higher compared with that of healthy controls (5.16±0.22 vs. 4.43±0.3 ng/mL, p=0.03). Although endoglin levels in synovial fluid were higher with respect to paired plasma samples, the difference was not significant (5.41±0.32 vs. 5.16±0.22 ng/mL, p=0.3). Additionally, plasma endoglin levels exhibited a positive correlation with synovial fluid endoglin levels (r=0.52, p=0.001). Further analysis revealed that plasma endoglin levels significantly correlated with disease severity (r=0.38, p=0.02). Furthermore, the synovial fluid levels of endoglin also positively correlated with disease severity (r=0.55, p=0.001).Conclusions: These findings indicate that endoglin in plasma and synovial fluid is correlated with progressive joint damage in knee OA. Endoglin is likely to be useful as a biomarker for determining disease severity and may play a possible role in the pathogenesis of osteoarthritis.</description><dc:title>Elevated Circulating and Synovial Fluid Endoglin Are Associated with Primary Knee Osteoarthritis Severity</dc:title><dc:creator>Sittisak Honsawek, Aree Tanavalee, Pongsak Yuktanandana</dc:creator><dc:identifier>10.1016/j.arcmed.2009.07.010</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>590</prism:startingPage><prism:endingPage>594</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001490/abstract?rss=yes"><title>Expression of Prostate Apoptosis Response (Par-4) Is Associated with Progesterone Receptor in Breast Cancer</title><link>http://www.arcmedres.com/article/PIIS0188440909001490/abstract?rss=yes</link><description>Background: The prostate apoptosis response (Par-4) gene encodes a proapoptotic protein that selectively induces apoptosis in cancer cells after diverse apoptotic stimuli. Par-4 expression and its association with other biomarkers have not been reported in breast cancer. The purpose of this study was to determine Par-4 expression in breast cancer samples and its association with other biomarkers and clinical factors (T-stage, age, nodal status).Methods: Paraffin-embedded section samples of breast cancer were evaluated by immunohistochemical analysis to determine Par-4, estrogen receptor (ER), progesterone receptor (PgR), c-erbB2, Ki67, p53 and bcl-2 expression. The correlation between Par-4 and the other biomarkers and clinical factors was determined by multivariate analysis.Results: Thirty five percent (n=21) of samples were PAR-4 positive and 64.4% (n=38) were negative. The hormonal status was 64% ER positive (n=38), 35% ER-negative (n=21) and 40.7% PgR positive (n=24), 59.3% PgR negative (n=35). The majority (90%) of the samples presented clear cytoplasmic localization and a small portion (10%) was cytoplasmic and nuclear. Univariate analysis indicates that the Par-4 expression has a significant inverse association (p=0.04) only with expression of PgR and not with the other variables analyzed. Normal breast tissue analyzed was negative for Par-4 immunostaining.Conclusions: Our results suggest that, in breast cancer, Par-4 plays a similar tumor suppressor gene role as reported in endometrial carcinoma</description><dc:title>Expression of Prostate Apoptosis Response (Par-4) Is Associated with Progesterone Receptor in Breast Cancer</dc:title><dc:creator>Pablo Zapata-Benavides, José L. Méndez-Vázquez, Talina R. González-Rocha, Diana E. Zamora-Avila, Moises A. Franco-Molina, Raúl Garza-Garza, Cristina Rodriguez-Padilla</dc:creator><dc:identifier>10.1016/j.arcmed.2009.08.007</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>595</prism:startingPage><prism:endingPage>599</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001507/abstract?rss=yes"><title>Influence of Genetic Polymorphism in Matrix Metalloproteinase-3 on Extent of Coronary Atherosclerosis and Risk of Coronary Artery Stenosis</title><link>http://www.arcmedres.com/article/PIIS0188440909001507/abstract?rss=yes</link><description>Background and Aims: Matrix metalloproteinase-3 (MMP3) is key member of the MMP family. It is known to be present in coronary atherosclerosis. Several studies have demonstrated that MMP-3 5A/6A polymorphism modifies each transcriptional activity in an allele-specific manner. We hypothesized that this polymorphism may be a risk factor for the development of coronary artery stenosis (CAS). We estimated the effect of MMP3 (5A/6A) gene polymorphism on CAS risk in an Iranian population.Methods: One hundred ninety patients with CAS and 200 healthy controls were in this study. MMP3 genotypes were determined by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP).Results: Significant differences between cases and controls were observed for MMP3 genotype frequencies (χ2=199.305, p&lt;0.001). The 6A allele was less frequently seen in the control group compared with the disease group (85.79 vs. 78%, 6A/6A+5A/6A vs. 5A/5A, p≤0.05). Association of this polymorphism with CAS severity was evaluated in the two groups, and distribution of the MMP3 genotype was not significantly different as compared with CAS severity (p&gt;0.05).Conclusions: These data imply involvement of the −1612 5A/6A polymorphism in CAS and also that the 6A/6A MMP-3 genotype is a genetic susceptibility factor for CAS (but does not affect disease severity).</description><dc:title>Influence of Genetic Polymorphism in Matrix Metalloproteinase-3 on Extent of Coronary Atherosclerosis and Risk of Coronary Artery Stenosis</dc:title><dc:creator>Morteza Seifi, Soudabeh Fallah, Mohsen Firoozrai</dc:creator><dc:identifier>10.1016/j.arcmed.2009.08.008</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>600</prism:startingPage><prism:endingPage>604</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001519/abstract?rss=yes"><title>Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) Is Increased in Human Left Ventricle after Acute Myocardial Infarction</title><link>http://www.arcmedres.com/article/PIIS0188440909001519/abstract?rss=yes</link><description>Background and Aims: Elevated activities of matrix metalloproteinases (MMPs) following acute myocardial infarction (AMI) have been shown to mediate ventricular remodeling. The extracellular MMP inducer (EMMPRIN) plays a key regulatory role for MMP activities. The aim of this study was to evaluate changes of EMMPRIN, MMP-2 and MMP-9 and determine the correlation between EMMPRIN expression and MMPs in human left ventricle after AMI.Methods: Immunohistochemistry for MMP-2, MMP-9 and EMMPRIN were performed postmortem in 15 human left ventricles including 10 patients with AMI and five normal subjects who were accident victims. Western blot was used to determine protein levels of MMP-2, MMP-9 and EMMPRIN. The correlation between EMMPRIN expression and MMPs was determined by linear regression.Results: Our results showed that there was slight EMMPRIN expression on the membranes of normal cardiac myocytes, whereas its expression strongly increased around the zone of necrosis in the AMI group. Compared with the control group, EMMPRIN (1.10±0.17 vs. 0.25±0.04, p&lt;0.001), MMP-2 (0.25±0.03 vs. 0.64±0.11, p&lt;0.001) and MMP-9 (0.16±0.03 vs. 0.39±0.07, p&lt;0.001) protein levels were significantly increased in the AMI group. The expression of MMP-2 (r2=0.82, p&lt;0.001), and MMP-9 (r2=0.424, p=0.041) were correlated with EMMPRIN expression in AMI patients.Conclusions: Our findings demonstrate for the first time that EMMPRIN expression increases in the human left ventricle after AMI. As one of the upregulators of local MMP expression, augmented expression of EMMPRIN may play a critical role in ventricular remodeling in AMI subjects.</description><dc:title>Extracellular Matrix Metalloproteinase Inducer (EMMPRIN) Is Increased in Human Left Ventricle after Acute Myocardial Infarction</dc:title><dc:creator>Ruqiong Nie, Shuanglun Xie, Bin Du, Xiaoyan Liu, Bingqing Deng, Jingfeng Wang</dc:creator><dc:identifier>10.1016/j.arcmed.2009.09.001</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>605</prism:startingPage><prism:endingPage>611</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001520/abstract?rss=yes"><title>Human Parvovirus B19 Infection in Patients with Coronary Atherosclerosis</title><link>http://www.arcmedres.com/article/PIIS0188440909001520/abstract?rss=yes</link><description>Background and Aims: The identification of possible pathogens for an infectious etiology of atherosclerotic coronary artery disease (CAD) is an expanding field. The present study was undertaken to explore the role of parvovirus B19, a potent infectious agent.Methods: A total of 565 patients were analyzed (90 patients with CAD, and 475 controls). Serologic analysis for human paravovirus B19 (B19) specific IgM and IgG was carried out in all patients. In addition, tissue specimens were obtained from five patients who received heart transplants. Direct in situ polymerase chain reaction (PCR) and immunocytochemistry were performed in the samples to localize B19 DNA.Results: Enzyme immunoassay showed that the seropositive rate of anti-B19 IgG in patients with CAD was 1.5- to 2.7-fold more frequent than in healthy controls. Clinical characteristics did not affect the prevalence of seropositivity for B19. However, anti-B19 IgM and B19-specific DNA were not detected in healthy or individuals with CAD. Furthermore, nonradioactive in situ PCR found that the majority of B19-specific DNA was located in the endothelial cells of the thickened intima.Conclusions: Our results first demonstrate a seroepidemiological and histopathological association between chronic B19 infection and CAD, suggesting that B19 infection may have a potential role in the pathogenesis of coronary atherosclerosis.</description><dc:title>Human Parvovirus B19 Infection in Patients with Coronary Atherosclerosis</dc:title><dc:creator>Shih-Chi Liu, Chia-Ti Tsai, Cho-Kai Wu, Meng-Fen Yu, Mu-Zon Wu, Liang-In Lin, Shoei-Shen Wang, Juey-Jen Hwang, Yung-Zu Tseng, Fu-Tien Chiang, Chuen-Den Tseng</dc:creator><dc:identifier>10.1016/j.arcmed.2009.09.002</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>612</prism:startingPage><prism:endingPage>617</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS018844090900188X/abstract?rss=yes"><title>Relationship Between Body Mass Index and Left Main Disease: The Obesity Paradox</title><link>http://www.arcmedres.com/article/PIIS018844090900188X/abstract?rss=yes</link><description>Background and Aims: Obesity is a well-known risk factor for development of diabetes, hypertension, and coronary artery disease. However, the obesity paradox shows that short-term outcome has been reported to be superior after revascularization in overweight patients. We conducted this study to examine this theory in patients who were candidates for coronary artery bypass graft and to determine if there is a relationship between obesity and the severity of coronary artery involvement and left main disease in Iranian patients.Methods: A total of 15,550 patients who had undergone isolated coronary artery bypass graft were studied retrospectively. All medical records of the aforementioned patients were derived from our hospital surgery data bank. Preoperative angiography was used for angiographic data.Results: After adjusting for confounding variables, we still found a significant relationship with higher BMI and lower prevalence of left main disease.Conclusions: We found that despite a higher prevalence of hypertension, diabetes mellitus, and dyslipidemia, overweight and obese patients who were candidates for coronary artery bypass graft surgery were significantly less likely to have left main disease according to preoperative angiography. This study suggests that obese patients are more likely to be referred for coronary artery bypass graft in earlier stages of coronary involvement.</description><dc:title>Relationship Between Body Mass Index and Left Main Disease: The Obesity Paradox</dc:title><dc:creator>Mahmood Shirzad, Abbasali Karimi, Samaneh Dowlatshahi, Seyed Hossein Ahmadi, Saeed Davoodi, Mehrab Marzban, Namvar Movahedi, Kyomars Abbasi, Mahmood Sheikh Fathollahi</dc:creator><dc:identifier>10.1016/j.arcmed.2009.10.005</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>618</prism:startingPage><prism:endingPage>624</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001817/abstract?rss=yes"><title>Study on TP53 Codon 72 Polymorphisms with Oral Carcinoma Susceptibility</title><link>http://www.arcmedres.com/article/PIIS0188440909001817/abstract?rss=yes</link><description>Background and Aims: Previous published data have implicated TP53 codon 72 polymorphisms as risk factors for various cancers. Growing bodies of studies have been conducted on the association of TP53 codon 72 polymorphisms with susceptibility to oral carcinoma and have yielded inconclusive results. The aim of the present study was to derive a more precise estimation of this relationship.Methods: We conducted a search in the relevant databases without a language limitation, covering all papers published until May 2009. The associated literature was acquired through deliberate searching and selected based on the established inclusion criteria for publications.Results: Nine studies including 1990 cases and 2074 controls were selected. Data were extracted and further analyzed using systematic meta-analyses. Results showed that no significant differences of oral cancer risk were found between individuals carrying homozygote Arg/Arg genotype and those carrying Pro/Pro genotype (OR: 0.96, 95% CI: 0.78−1.19). Likewise, no evidence indicated that individuals with Arg/Arg genotype have a significant risk of oral cancer compared with those with a combined Pro genotype (Arg/Pro+Pro/Pro) (OR: 0.98, 95% CI: 0.85−1.12). Similarly, individuals with a combined Arg genotype (Arg/Pro+Arg/Arg) do not have a marked increased or decreased susceptibility to oral cancer relative to those with homozygote Pro/Pro genotype (OR: 1.00, 95% CI: 0.83−1.21). Moreover, when stratifying for race, results were similar among Asians or Caucasians. In addition, TP53 codon 72 polymorphisms may not associate with oral cancer risks in smokers and HPV infection status.Conclusions: No evidence suggests that TP53 codon 72 polymorphisms may be a risk factor for oral carcinoma.</description><dc:title>Study on TP53 Codon 72 Polymorphisms with Oral Carcinoma Susceptibility</dc:title><dc:creator>Xian-Lu Zhuo, Qi Li, Yan Zhou, Lei Cai, Zhao-Lan Xiang, Wei Yuan, Xue-Yuan Zhang</dc:creator><dc:identifier>10.1016/j.arcmed.2009.09.004</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Original Articles</prism:section><prism:startingPage>625</prism:startingPage><prism:endingPage>634</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001489/abstract?rss=yes"><title>Portopulmonary Hypertension in Children. A Study In Pediatric Autopsies</title><link>http://www.arcmedres.com/article/PIIS0188440909001489/abstract?rss=yes</link><description>Background and Aims: The relative frequency and risk factors of portopulmonary hypertension in children have not been defined with precision. The few published reports refer to isolated cases or small series from selected populations. The development of pulmonary hypertension in patients with portal hypertension is seldom suspected or documented during life. The examination of autopsy material can identify these cases because pulmonary hypertension produces characteristic histological changes in the pulmonary vasculature.Methods: Autopsy cases with evidence of portal hypertension were retrieved. Slides of pulmonary tissue from these cases were examined in search of histopathological changes of hypertensive arteriopathyResults: Seventy six cases of portal hypertension were identified among 7060 autopsies collected between January 1971 and January 2008 (1.07%). Four cases with histopathological evidence of pulmonary hypertension were identified. This represents 5.2% of all cases with portal hypertension. These four patients were females in late childhood or adolescence with idiopathic portal hypertension. Pulmonary hypertension was not diagnosed during their lifetime.Conclusions: Idiopathic portal hypertension in adolescent girls should be considered a risk factor for the development of portopulmonary hypertension, very likely as a consequence of the functional preservation of hepatic tissue that allows a prolonged survival. An oriented search for early signs of pulmonary hypertension in these patients would appear advisable in order to install timely treatment.</description><dc:title>Portopulmonary Hypertension in Children. A Study In Pediatric Autopsies</dc:title><dc:creator>Cecilia Ridaura-Sanz, Carmen Mejía-Hernández, Eduardo López-Corella</dc:creator><dc:identifier>10.1016/j.arcmed.2009.08.006</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Brief Report</prism:section><prism:startingPage>635</prism:startingPage><prism:endingPage>639</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909001866/abstract?rss=yes"><title>Iron, γ-Glutamyltransferase, and Atherosclerosis</title><link>http://www.arcmedres.com/article/PIIS0188440909001866/abstract?rss=yes</link><description>Turgut and colleagues  proposed that an increase in serum levels of γ-glutamyltransferase (GGT), even within its normal range, may represent a promising biohumoral predictor for atherosclerosis, and supplementary GGT determination to conventional testing may have potential implications for screening individuals at increased cardiovascular risk who may benefit from prophylactic measures and require enhanced therapeutic effort. We agree and further suggest that the pathogenic role of GGT in atherosclerosis may be related to elevated body iron stores.</description><dc:title>Iron, γ-Glutamyltransferase, and Atherosclerosis</dc:title><dc:creator>Luca Mascitelli, Francesca Pezzetta, Mark R. Goldstein</dc:creator><dc:identifier>10.1016/j.arcmed.2009.10.003</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Letter to the Editor</prism:section><prism:startingPage>640</prism:startingPage><prism:endingPage>640</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909002185/abstract?rss=yes"><title>Guide for Authors</title><link>http://www.arcmedres.com/article/PIIS0188440909002185/abstract?rss=yes</link><description></description><dc:title>Guide for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0188-4409(09)00218-5</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section></prism:section><prism:startingPage>IBC</prism:startingPage><prism:endingPage>IBC</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909002057/abstract?rss=yes"><title>Editorial Board</title><link>http://www.arcmedres.com/article/PIIS0188440909002057/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0188-4409(09)00205-7</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A1</prism:startingPage><prism:endingPage>A1</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909002069/abstract?rss=yes"><title>Table of Contents</title><link>http://www.arcmedres.com/article/PIIS0188440909002069/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0188-4409(09)00206-9</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A2</prism:startingPage><prism:endingPage>A3</prism:endingPage></item><item rdf:about="http://www.arcmedres.com/article/PIIS0188440909002173/abstract?rss=yes"><title>Guide for Authors</title><link>http://www.arcmedres.com/article/PIIS0188440909002173/abstract?rss=yes</link><description></description><dc:title>Guide for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S0188-4409(09)00217-3</dc:identifier><dc:source>Archives of Medical Research 40, 7 (2009)</dc:source><dc:date>2009-10-01</dc:date><prism:publicationName>Archives of Medical Research</prism:publicationName><prism:publicationDate>2009-10-01</prism:publicationDate><prism:volume>40</prism:volume><prism:number>7</prism:number><prism:issueIdentifier>S0188-4409(09)X0007-X</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A7</prism:startingPage><prism:endingPage>A8</prism:endingPage></item></rdf:RDF>